ライフサイエンスコーパス: Sertoli

1 Sertoli cells (SCs) regulate testicular fate in the diff

2 Sertoli cells are considered the "supporting cells" of t

3 Sertoli cells produce GDNF and other growth factors and

4 Sertoli cells, can function as non-professional toleroge

5 Sertoli cells, the epithelial cell type within testis co

6 It has been viewed as a Sertoli-cell driven process, but growing evidence sugges

7 Sin3A-deleted testes exhibit a Sertoli-cell only phenotype, consistent with the absolut

8 ratubular germ cell neoplasia was found in a Sertoli cell adenoma.

9 ule severely reduced Sox9 transcription in a Sertoli cell line.

10 tate prior to transdifferentiating towards a Sertoli cell fate.

11 binase-expressing mice and in testis using a Sertoli cell Cre recombinase-expressing mouse.

12 nfirming a requirement for PPARD in accurate Sertoli cell function.

13 led to a dis-organization of F-actin across Sertoli cell cytosol, causing truncation of actin microf

14 ed by specialized junctions between adjacent Sertoli cells in the seminiferous epithelium near the ba

15 estis barrier (BTB), formed between adjacent Sertoli cells, undergoes extensive remodeling to facilit

16 lood-testis barrier (BTB) formed by adjacent Sertoli cells is composed of coexisting tight junction (

17 mary pre-pubertal Sertoli cells and in adult Sertoli line, TLR4\NOD1 and NOD2 crosstalk converged in

18 Ex vivo, ibuprofen also affected Sertoli cell by suppressing AMH production and mRNA expr

19 of potential feminizing genes, DMRT1 allows Sertoli cells to participate in RA signaling, which is e

20 Although Sertoli cells are a driving force in the de novo formati

21 as juvenile granulosa-cell, Leydig-cell, and Sertoli-cell tumours).

22 rget genes can differ between germ cells and Sertoli cells.

23 changes, including paratesticular cysts and Sertoli cell adenomas.

24 , we observed progressive germ cell loss and Sertoli cell only tubules in Lkb1(cko) testes from mice

25 is-to-ovary genetic reprogramming occurs and Sertoli cells transdifferentiate into granulosa-like cel

26 germ cell (Dazl), proliferating (PCNA), and Sertoli cell populations, and quantitated levels of apop

27 s in protein distribution at the Sertoli and Sertoli-germ-cell cell interface and by phosphorylation

28 ted spermatogonia, primary spermatocytes and Sertoli cells in the testis, resulting in cell death and

29 tercellular spaces between spermatogenic and Sertoli cells as well as the spermatid deformities.

30 cell-cell adhesion between spermatogenic and Sertoli cells through its interaction with NECL4 on Sert

31 o the pachytene stage, as spermatogonial and Sertoli cells were unaffected in knockout mice.

32 c failure that presents clinically in men as Sertoli-cell only (SCO) pathology of the testis.

33 tor cells acquire SOX9 expression and become Sertoli cells that form testis cords, whereas the remain

34 Although these changes are usually benign, Sertoli adenomas can sometimes harbor premalignant lesio

35 ith the formation of tight junctions between Sertoli cells during postnatal development.

36 ier created by specialized junctions between Sertoli cells near the basement membrane confers an immu

37 ages revealed a normal BTB structure between Sertoli cells in the BT-IgSF-KO mice, we conclude that i

38 A deficiency of RDH10 in both Sertoli and germ cells in juvenile mice results in a blo

39 quired for the lineage specification of both Sertoli and granulosa cells by repressing Sf1 expression

40 Furthermore, differentiation of both Sertoli and granulosa cells was blocked when Wt1 was del

41 ignificantly reduced Leydig cell numbers but Sertoli cell specific AR ablation had no effect.

42 gocytic clearance of apoptotic germ cells by Sertoli cells is essential for spermatogenesis, little o

43 gocytic clearance of apoptotic germ cells by Sertoli cells is vital for germ cell development and dif

44 gocytic clearance of apoptotic germ cells by Sertoli cells lining the seminiferous epithelium.

45 ficient clearance of apoptotic germ cells by Sertoli cells using LAP.Although phagocytic clearance of

46 of the seminiferous epithelium delimited by Sertoli cells and peritubular myoid (PM) cells.

47 s3, CRB3) is a polarity protein expressed by Sertoli and germ cells at the basal compartment in the s

48 t testis, Rai14 was found to be expressed by Sertoli and germ cells, structurally associated with act

49 cycle (i) RALDH-dependent synthesis of RA by Sertoli cells (SC), the supporting cells of the germ cel

50 nal characteristics of large-cell calcifying Sertoli cell tumors of the testes (LCCSCTs).

51 conserved among mammals and that we called 'Sertoli Cell Signature' (SCS).

52 ated N-glycans that participate in germ cell-Sertoli cell adhesion.

53 ons indicate that BSG may act as a germ cell-Sertoli cell attachment molecule.

54 e spermatocyte stage, BSG-mediated germ cell-Sertoli cell interactions appear to be necessary for int

55 Supporting cells (Sertoli and granulosa) and steroidogenic cells (Leydig a

56 s exert deleterious effects on Leydig cells, Sertoli cells, and germ cells via very different mechani

57 In contrast, Sertoli cell-only tubules were detected in parallel xeno

58 alpha) since germ cells are known to control Sertoli cell production of this cytokine, and if yes, ho

59 vel transcription factors likely controlling Sertoli cell differentiation.

60 Using primary cultured Sertoli cells as an in vitro model that mimics the BTB i

61 rd elongation and expansion due to decreased Sertoli cell proliferation.

62 ce, and these were associated with decreased Sertoli cell number in Ppard(+/+) mice.

63 74%) and low-signal-intensity, well-defined Sertoli cell adenomas (26 of 46 testes, 56%).

64 mium because its knockdown would desensitize Sertoli cells to cadmium-induced TJ barrier disruption.

65 These changes destabilized Sertoli cell blood-testis barrier (BTB) integrity.

66 cal role in mammalian gonads is to determine Sertoli cells, we correlated this genomic signature with

67 esis and are at increased risk of developing Sertoli cell tumors.

68 These differentiated Sertoli cells remained mitotically active when cultured

69 dysgenesis (Leydig cell aggregation, ectopic Sertoli cells, malformed seminiferous cords) is not evid

70 ocal aggregation of Leydig cells and ectopic Sertoli cells (SC).

71 re, and cooperated with endogenous embryonic Sertoli and primordial germ cells in the generation of t

72 lar-like structures, and expressed embryonic Sertoli-specific markers.

73 onstrate the generation of induced embryonic Sertoli-like cells (ieSCs) by ectopic expression of five

74 codes a core NMD factor, in murine embryonic Sertoli cells (SCs) leads to severe testicular atrophy a

75 erm cells inside tubules lined by epithelial Sertoli cells.

76 al-time polymerase chain reaction to examine Sertoli and germ cell markers on rat testes and human fe

77 ycans on glycoproteins, thereby facilitating Sertoli-germ cell attachment at a particular stage of sp

78 substance (MIS), which is produced by fetal Sertoli cells shortly after commitment of the bipotentia

79 to a genomic bar code of the fate of foetal Sertoli cells.

80 ELMO1, respectively) were also important for Sertoli-cell-mediated engulfment.

81 iotic transitions are coordinated by RA from Sertoli (somatic) cells.

82 Primary and immortalized GAR22beta(-/-) Sertoli cells moved faster than wild-type cells.

83 , receptors, and integrins required for germ-Sertoli cell adhesion and dynamic junctional restructuri

84 Human Sertoli cells obtained from men at ages 15, 23, 36 and 4

85 PFOS induces human Sertoli cell injury which can be rescued by overexpressi

86 Herein, we maintained human Sertoli cells in a mitotically active state in vitro, th

87 rovide evidence that ZIKV infection of human Sertoli cells, which are an important component of the s

88 f P-glycoprotein by RNAi was found to impede Sertoli cell BTB function, making the tight junction (TJ

89 r knockdown by RNAi was also found to impede Sertoli cell-cell GJ communication, disrupting protein d

90 In Sertoli cell cultures with established permeability barr

91 A knockdown (KD) of plastin 3 in Sertoli cells by RNA interference using an in vitro mode

92 Transgenic mice expressing miR-471-5p in Sertoli cells show increased germ cell apoptosis and com

93 helial cells and germ cells, while absent in Sertoli cells or BTB site.

94 we found that Notch signaling was active in Sertoli cells at various fetal, neonatal, and adult stag

95 astly, the BEST1 promoter was also active in Sertoli cells of the testis in transgenic mice where SOX

96 emonstrate that Notch signaling is active in Sertoli cells throughout development and that proper reg

97 importance, a knockdown of laminin alpha2 in Sertoli cells was shown to induce the Sertoli cell tight

98 was sparsely expressed in germ cells and in Sertoli cells.

99 of proliferating cellular nuclear antigen in Sertoli cells were observed in Ppard(+/+) mice as compar

100 However, a knockdown of Cx43 in Sertoli cells by RNAi significantly reduced the kinetics

101 xt investigated if overexpression of Cx43 in Sertoli cells could rescue the PFOS-induced cell injury.

102 Indeed, overexpression of Cx43 in Sertoli cells with an established TJ-barrier blocked the

103 der than 10 weeks, accompanied by defects in Sertoli cell polarity and testicular junctional complexe

104 testes and found that an RDH10 deficiency in Sertoli cells, but not in germ cells, results in a mild

105 in which Zbtb20 was specifically deleted in Sertoli cells.

106 naling components have long been detected in Sertoli and germ cells in the developing and mature test

107 In testis, RA acts directly in Sertoli, Leydig and pre-meiotic germ cells.

108 uncover a selective requirement for ELMO1 in Sertoli-cell-mediated removal of apoptotic germ cells an

109 ve regulatory sites around genes enriched in Sertoli and pregranulosa cells; however, active enhancer

110 led several potential modifiers expressed in Sertoli cells at the time of testis determination in mic

111 e found that WT1 and KDR are co-expressed in Sertoli cells of the testes and somatic cells of embryon

112 ia also disrupts cyclical gene expression in Sertoli cells.

113 in the re-organization of actin filaments in Sertoli cells during the epithelial cycle, participating

114 perturbed organization of actin filaments in Sertoli cells, disruption of the blood-testis barrier an

115 ta on inflammasome expression or function in Sertoli cells.

116 The absence of BT-IgSF in Sertoli cells in both global and conditional mouse mutan

117 Its involvement in Sertoli-germ cell adhesion was substantiated in studies

118 uration, and formation of tight junctions in Sertoli cells, thus confirming a requirement for PPARD i

119 concomitant activation of CTNNB1 and KRAS in Sertoli cells also caused testicular granulosa cell tumo

120 lls in the testes, but at very low levels in Sertoli cells.

121 permatogenesis, its specific localization in Sertoli cells makes Zbtb20 a useful marker for the ident

122 Here, we found that it is localized in Sertoli cells at the blood-testis barrier (BTB) and at t

123 Arid4a and Arid4b are expressed mainly in Sertoli cells of testes, which implies that their roles

124 tions in the organization of microtubules in Sertoli cells and a loss of barrier integrity despite a

125 ing actin microfilaments and microtubules in Sertoli cells so that they failed to support cell adhesi

126 e, intracellular domain of NOTCH1 (NICD1) in Sertoli cells.

127 1 is required in fetal germ cells but not in Sertoli cells to prevent teratoma formation.

128 orphology and the position of the nucleus in Sertoli cells were normal, however, in the nesprin-3-kno

129 s would be modulated through this pathway in Sertoli cells.

130 in, or the use of a synthetic F5 peptide, in Sertoli cells with an established functional blood-testi

131 elial ovarian tumors (29%), predominantly in Sertoli-Leydig cell tumors (26 of 43, or 60%), including

132 This was most prominent in Sertoli cells of the testis, in which nesprin-3 is requi

133 A knockdown of Rai14 in Sertoli cells cultured in vitro by RNAi was found to per

134 SHR ablation also caused small reductions in Sertoli cell numbers up to day 20 with more marked effec

135 drive expression of a transgenic reporter in Sertoli cells.

136 ate that Ins2 is a direct target of Rhox5 in Sertoli cells, and we show that this regulation is physi

137 CRB3 knockdown (KD) by RNAi in Sertoli cells with an established tight junction (TJ)-pe

138 of testes, which implies that their roles in Sertoli cell function are to support spermatogenesis and

139 k180, LC3, Atg12, Becn1, Rab5 and Rubicon in Sertoli cells.

140 ere, we demonstrate that deletion of Shp2 in Sertoli cells results in infertility in mice.

141 e mechanisms controlled by LKB1 signaling in Sertoli cell functions and testicular biology have not b

142 physiological function of NOTCH signaling in Sertoli cells has not been demonstrated.

143 We conclude that NOTCH signaling in Sertoli cells is required for proper regulation of the t

144 that proper regulation of Notch signaling in Sertoli cells is required for the maintenance of gonocyt

145 constitutively activating NOTCH signaling in Sertoli cells leads to premature differentiation of all

146 central component of TGF-beta signaling, in Sertoli cells led to testis cord dysgenesis and prolifer

147 ), a crucial mediator of NOTCH signaling, in Sertoli cells using Amh-cre.

148 of the transcription factors SRY and SOX9 in Sertoli cells lead to human sex reversal diseases with a

149 Here we show that after ablation of Sox9 in Sertoli cells of adult, fertile Sox8(-/-) mice, testis-t

150 ressing its dominant-negative mutant T17N in Sertoli cell epithelium was shown to block the TGF-beta3

151 c deletion of transcription factor Zbtb20 in Sertoli cells has no apparent influence on spermatogenes

152 stis barrier (BTB), PFOS was found to induce Sertoli cell injury by perturbing actin cytoskeleton thr

153 PFOS was found to induce Sertoli cell injury through disruptive effects on actin

154 Interestingly, PFOS-induced Sertoli cell injury associated with a down-regulation of

155 rected], was found to block the PFOS-induced Sertoli cell injury by rescuing the PFOS-induced F-actin

156 PFOS induces Sertoli cell injury using testicular cells isolated from

157 osa cells can reprogram granulosa cells into Sertoli cells.

158 transdifferentiation of granulosa cells into Sertoli-like cells in the adult mouse ovary.

159 mmed juvenile and adult granulosa cells into Sertoli-like cells, triggering formation of structures r

160 not exclusive, source of RA in the testes is Sertoli cells.

161 leads to malfunction of the somatic (Leydig, Sertoli) cells and consequent downstream TDS disorders.

162 gnaling protein that is required to maintain Sertoli cell function and could serve as a novel target

163 ion of bipotential precursor cells into male Sertoli cells or female granulosa cells.

164 sexual cell-fate reprogramming in which male Sertoli cells transdifferentiate into their female equiv

165 In ARKO mice Sertoli cell numbers were reduced at all ages from birth

166 of PPARD inhibited proliferation of a mouse Sertoli cell line, TM4, and an inverse agonist of PPARD

167 NOD1 and NOD2 expression in human and mouse Sertoli cells.

168 s of the DMRT1 transcription factor in mouse Sertoli cells, even in adults, activates Foxl2 and repro

169 Changes in PGD2 secretion in juvenile mouse Sertoli cells (SC5 cells) were measured using an ELISA.

170 staglandin D2 (PGD2) inhibition in SC5 mouse Sertoli cells, evidence of binding at the COX-2 active s

171 We found that mutant Sertoli cells were morphologically normal before and aft

172 Germ cell-specific, but not Sertoli cell-specific Nhe8 disruption recapitulated the

173 tion of this approach, we identified a novel Sertoli cell enhancer upstream of Wt1, and used it to dr

174 correctly depict the presence or absence of Sertoli cell adenomas in 19 of 23 testes (83%).

175 erstitial progenitors, through the action of Sertoli cell-derived Hedgehog signals, become positive f

176 s development is solely under the control of Sertoli cells, by uncovering an active and essential rol

177 unction restructuring in primary cultures of Sertoli cells isolated from rat testes that formed a TJ-

178 cells, with likely secondary degeneration of Sertoli cells, including the blood-testis barrier, which

179 s, SOX9 is required for the determination of Sertoli cells that orchestrate testis morphogenesis.

180 nsequently, this prevented the disruption of Sertoli cell TJ permeability barrier and redistribution

181 fects are correlated with a dysregulation of Sertoli-expressed genes that are required for germ cell

182 permatogenesis by modulating the function of Sertoli cells during early testis development.

183 20 a useful marker for the identification of Sertoli cells in seminiferous tubules.

184 anisms governing the functional integrity of Sertoli cells have remained largely unexplored.

185 Further investigation of Sertoli cells treated with IL-1alpha revealed striking c

186 oring junction) function along the length of Sertoli cell in the testis.

187 tion and MNG induction appears to be loss of Sertoli cell-germ cell membrane adhesion, probably due t

188 I of meiosis but does inhibit maturation of Sertoli cells, which continue to express the immaturity

189 Herein, using an in vitro model of Sertoli cell blood-testis barrier (BTB), PFOS was found

190 was localized specifically in the nuclei of Sertoli cells in seminiferous tubules.

191 ation of plectin to the nuclear perimeter of Sertoli cells, the resulting link between the nuclear en

192 BTB in the rat testis and the phenotypes of Sertoli cell-conditional Cx43 knockout mice share many o

193 nockout mice (SCSKO), a normal population of Sertoli cells was observed, but the blood-testis barrier

194 d in 37% of patients despite a prevalence of Sertoli cell-only pattern on preoperative biopsy.

195 ysis revealed that the expression program of Sertoli cells is altered upon inactivation of Sin3A in g

196 atory pathways involved in the regulation of Sertoli cell function and male fertility.

197 e for Akap9 in the coordinated regulation of Sertoli cells in the testis.

198 lity to reproduce is completely dependent on Sertoli cells.

199 major TGF-beta protein that acts directly on Sertoli cells.

200 strate PFOS exerts its disruptive effects on Sertoli cell function downstream through Akt1/2.

201 cells through its interaction with NECL4 on Sertoli cells.

202 ed by H3K27ac were enriched proximal to only Sertoli-enriched genes.

203 ating step for 1 month were transferred onto Sertoli feeder cells, they differentiated into functiona

204 an testes, the blood-testis barrier (BTB) or Sertoli cell barrier created by specialized junctions be

205 t with NSun2 in spermatogonial stem cells or Sertoli cells.

206 mrt1 is selectively mutated in germ cells or Sertoli cells.

207 equired for the survival of trophectoderm or Sertoli cells.

208 (GODZ; also known as DHHC3) and its paralog Sertoli cell gene with a zinc finger domain-beta (SERZ-b

209 ired phagocytosis by specialized phagocytes: Sertoli cells and the retinal pigmented epithelium (RPE)

210 Interestingly, phenotypic Sertoli cell dysfunction in the Arid4a(-/-)Arid4b(+/-) m

211 re the basal membranes of adjacent polarized Sertoli cells form a niche for the proliferating spermat

212 Neonatal porcine Sertoli cells (NPSC) are immune privileged cells showing

213 provide evidence, based on an embryonic pre-Sertoli cell line, that this domain functions at a thres

214 ending are unaffected in a rat embryonic pre-Sertoli cell line, the variants exhibited selective defe

215 pe A, Int, B spermatogonia as well as in pre-Sertoli cells and Leydig cells but was undetectable in s

216 s is initiated when expression of Sry in pre-Sertoli cells directs the gonad toward a male-specific f

217 tiated by upregulation of Sox9 by SRY in pre-Sertoli cells.

218 ific siRNA duplexes was performed in primary Sertoli cell cultures with an established TJ permeabilit

219 n impaired the cell junctions of the primary Sertoli cells and failed to support the clonal formation

220 y restores the cell junctions of the primary Sertoli cells and the clonal formation of SSCs.

221 Using primary Sertoli cells cultured in vitro with an established tigh

222 ession of structural proteins and protecting Sertoli cells from early apoptosis.

223 We found that in primary pre-pubertal Sertoli cells and in adult Sertoli line, TLR4\NOD1 and N

224 We find that androgen regulates Sertoli cell phagocytosis by controlling expression of m

225 -testis barrier (BTB) involved in regulating Sertoli cell adhesion via its effects on the occludin-zo

226 n reducing occupancy of DNA sites regulating Sertoli-cell differentiation [the testis-specific SRY-bo

227 en in adults, activates Foxl2 and reprograms Sertoli cells into granulosa cells.

228 nal formation of SSCs co-cultured with SCSKO Sertoli cells.

229 Several Sertoli cell-expressed genes, such as Gdnf and Cyp26b1,

230 s strands of tight junctions between somatic Sertoli cells that restricts solutes from crossing the p

231 Its key step, Sertoli cell differentiation in the embryonic gonadal ri

232 sites during sex determination, we subjected Sertoli cells from mouse fetal testes to DNaseI-seq and

233 a without direct contact with the supporting Sertoli cells, we show that haploid spermatids express t

234 ired in both germ cells and their supporting Sertoli cells.

235 recursor cells differentiate into testicular Sertoli cells or ovarian granulosa cells.

236 In the testis, Sertoli cells are the key niche cells directing the popu

237 This study is proof of concept that Sertoli cells, upon specific stimulation, could particip

238 Here the authors show that Sertoli cells employ LC3-associated phagocytosis (LAP) b

239 androgen receptor (AR) knockout mice and the Sertoli cell-specific RB knockout mice.

240 in the granulosa cells of the ovary and the Sertoli cells of the testis.

241 rmatid (apical ES) interface, as well as the Sertoli cell-cell (basal ES) interface at the blood-test

242 d via changes in protein distribution at the Sertoli and Sertoli-germ-cell cell interface and by phos

243 These effects at the Sertoli cell barrier were mediated, in part, by epiderma

244 ed by changes in F-actin organization at the Sertoli cell BTB in vitro and in vivo, associated with a

245 turn led to protein mis-localization at the Sertoli cell BTB.

246 uced the rate of actin polymerization at the Sertoli cell BTB.

247 ns at the tight junction and basal ES at the Sertoli cell BTB.

248 This includes ES at the Sertoli cell-elongating/elongated spermatid interface, w

249 pecific, actin-rich adherens junction at the Sertoli cell-spermatid interface) to coordinate cellular

250 n led to a redistribution of occludin at the Sertoli-Sertoli cell interface, moving from cell membran

251 istribution of TJ-associated proteins at the Sertoli-Sertoli cell interface.

252 (ii) anchoring junction restructuring at the Sertoli-spermatid interface induced by adjudin which mim

253 testes, most notably at the apical ES at the Sertoli-spermatid interface, and expressed stage-specifi

254 posits that MGCA are sequestered behind the Sertoli cell barrier in seminiferous tubules.

255 by the blood-testis barrier, also called the Sertoli cell (SC) barrier (SCB).

256 rmer promoting and the latter disrupting the Sertoli cell tight junction-permeability barrier functio

257 ecise organization of binding motifs for the Sertoli cell reprogramming factors SOX9, GATA4 and DMRT1

258 rier, recapitulated the defects found in the Sertoli cell-specific androgen receptor (AR) knockout mi

259 KitL localization is affected in the Sertoli cells of the KitL(L263A/L263A) testis and testis

260 ressed sFRP1 using lentiviral vectors in the Sertoli-germ cell coculture system.

261 ha2 in Sertoli cells was shown to induce the Sertoli cell tight junction permeability barrier disrupt

262 of bundles of actin microfilaments near the Sertoli cell plasma membrane.

263 transcription factor for maintenance of the Sertoli cell phenotype.

264 e (FSH) acts through receptors (FSHR) on the Sertoli cell to stimulate spermatogenesis while androgen

265 quitously (ARKO mice) or specifically on the Sertoli cells (SCARKO mice).

266 testis growth through receptors (AR) on the Sertoli cells, Leydig cells and peritubular myoid cells.

267 L-1alpha (100 pg/ml) was shown to "open" the Sertoli cell barrier when its integrity was assessed by

268 form localized immune complexes outside the Sertoli cell barrier.

269 ed in vitro by RNAi was found to perturb the Sertoli cell tight junction-permeability function in vit

270 n of rictor by RNAi was found to perturb the Sertoli cell TJ-barrier function in vitro and the BTB in

271 PFOS perturbed the Sertoli cell tight junction (TJ)-permeability barrier, c

272 The removal of calcium by EGTA perturbed the Sertoli cell tight junction barrier, but calcium repleti

273 a transient loss of plastin 3 perturbed the Sertoli cell tight junction-permeability barrier, mediat

274 ter the knockdown of both Cx43 and PKP2, the Sertoli cell TJ barrier function was perturbed transient

275 which is known as apical ES and possibly the Sertoli-Sertoli cell interface, known as basal ES, at th

276 t overexpression of Cx43 indeed resealed the Sertoli cell tight junction-permeability barrier based o

277 Throughout spermatogenesis, the Sertoli cell blood-testis barrier (BTB) is strictly regu

278 icrofilament, thereby failing to support the Sertoli cell morphology and adhesion protein complexes (

279 Although we show that the Sertoli cells of the testis secrete insulin protein, thi

280 In light of new evidence that the Sertoli cells of the testis secrete insulin, it is curre

281 on than androgen action mediated through the Sertoli cells although androgen action through other cel

282 ndent on FSH and androgen action through the Sertoli cells.

283 the actions of FSH and androgen through the Sertoli cells.

284 ecruitment of actin-related protein 3 to the Sertoli cell-cell interface, where it became more tightl

285 nd GATA4, whereas SOX9 was restricted to the Sertoli precursors and LHX9 to the coelomic epithelium a

286 ES is restricted to the Sertoli-spermatid (apical ES) interface, as well as the

287 Large cysts of germ cells transit the Sertoli cell tight junctions (SCTJs) without compromisin

288 These Sertoli-like cells facilitated neuronal differentiation

289 ntation in the epithelium, and a "tightened" Sertoli cell TJ permeability barrier, supporting the rol

290 y increases the adhesion of CHO cells to TM4 Sertoli cells.

291 l-cell adhesions of developing germ cells to Sertoli nurse cells, with likely secondary degeneration

292 e caused, at least partly, by disruptions to Sertoli cell function and increased germ cell apoptosis,

293 germ cell membrane adhesion, probably due to Sertoli cell microfilament redistribution.

294 s, there is evidence of pregranulosa cell-to-Sertoli cell transdifferentiation near birth, following

295 e fetal Leydig cells that acts directly upon Sertoli cells to promote their proliferation during late

296 By using Sertoli cells cultured in vitro with an established TJ p

297 Androgen signaling via Sertoli cells (SCs) is essential for complete spermatoge

298 The use of an in vitro Sertoli cell barrier to describe how ZIKV or inflammator

299 When Sertoli cells were isolated from Sprague-Dawley rats and

300 interactions of other testicular cells with Sertoli cells and to test novel antivirals for clearing