Barrier properties of testis microvessels.

Holash, Jocelyn; Harik, Sami I.; Perry, George; Stewart, Patricia A.

doi:10.1073/pnas.90.23.11069

Cited by 122 publications

(80 citation statements)

References 48 publications

(55 reference statements)

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“…This may be attributable to the glia-like phenotype of these cells, since they express high levels of glutamine synthetase, an enzyme that rapidly metabolizes any available glutamate to glutamine. 16,55 We do not believe that this disparity is attributable to delays in fixation of the testis, since such delays in fixation normally cause a rise in glutamate levels in tissues that express glutamine synthetase. 26 It might be expected that other cells that express the glutamate-synthesizing enzyme glutamate dehydrogenase, such as the Sertoli cells, 56 might contain detectable pools of glutamate.…”

Section: Distribution and Possible Roles Of Glutamate In The Testismentioning

confidence: 97%

“…The current study was initiated because the testis shares clear homologies to the mammalian brain, in the possession of a blood-testis barrier 15 that is homologous to, but structurally distinct from, the blood-brain barrier. The blood-testis barrier is predominantly formed by tight junctions between Sertoli cells; 16 however, Leydig cells in the interstitial tissues that share antigenic homologies to astrocytes 16,17 may also influence barrier properties. The blood-brain barrier is induced by astrocytes and is constituted by tight junctions between endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

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Expression of multiple glutamate transporter splice variants in the rodent testis

Lee¹,

Anderson²,

Barnett³

et al. 2010

Asian J Androl

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Glutamate is a regulated molecule in the mammalian testis. Extracellular regulation of glutamate in the body is determined largely by the expression of plasmalemmal glutamate transporters. We have examined by PCR, western blotting and immunocytochemistry the expression of a panel of sodium-dependent plasmalemmal glutamate transporters in the rat testis. Proteins examined included: glutamate aspartate transporter (GLAST), glutamate transporter 1 (GLT1), excitatory amino acid carrier 1 (EAAC1), excitatory amino acid transporter 4 (EAAT4) and EAAT5. We demonstrate that many of the glutamate transporters in the testis are alternately spliced. GLAST is present as exon-3-and exon-9-skipping forms. GLT1 was similarly present as the alternately spliced forms GLT1b and GLT1c, whereas the abundant brain form (GLT1a) was detectable only at the mRNA level. EAAT5 was also strongly expressed, whereas EAAC1 and EAAT4 were absent. These patterns of expression were compared with the patterns of endogenous glutamate localization and with patterns of D-aspartate accumulation, as assessed by immunocytochemistry. The presence of multiple glutamate transporters in the testis, including unusually spliced forms, suggests that glutamate homeostasis may be critical in this organ. The apparent presence of many of these transporters in the testis and sperm may indicate a need for glutamate transport by such cells.

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Section: Distribution and Possible Roles Of Glutamate In The Testismentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Expression of multiple glutamate transporter splice variants in the rodent testis

Lee¹,

Anderson²,

Barnett³

et al. 2010

Asian J Androl

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“…Northern blot analysis with poly(A) + mRNA revealed transgene expression in the brain and a weak signal in testes of transgenic mice (data not shown). In addition, weak expression of the endogenous GFAP gene was found in testes as described previously (Holash et al, 1993). The cellular distribution pattern of transgene expression was assessed by in situ hybridization.…”

Section: Analysis Of Transgene Expressionmentioning

confidence: 99%

Development and malignant progression of astrocytomas in GFAP-v-src transgenic mice

et al. 1997

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We have generated a transgenic mouse model for astrocytoma by expressing the v-src kinase under control of the glial ®brillary acidic protein (GFAP) gene regulatory elements in astrocytes. Abnormal astrogliosis was observed in all transgenic animals already at 2 weeks postnatally, frequently followed by the development of dysplastic changes. Later, small proliferative foci arose, and overt astrocytoma developed in the brain and spinal cord in 14.4% of mice after a follow up time of 65 weeks. While early lesions were histologically consistent with low-grade astrocytoma, at later stages most tumors were highly mitotic and frankly malignant. Vascular endothelial growth factor (VEGF) was expressed by tumor cells already at early stages, suggesting induction by v-src, and it was most pronounced in pseudopalisading cells surrounding necrotic areas, implying additional upregulation by hypoxia. In larger lesions, mitotic activity and expression of¯k-1, the cognate receptor of VEGF were induced in endothelial cells. Therefore, end-stage tumors mimicked the morphological and molecular characteristics of human glioblastoma multiforme. Time course and stochastic nature of the process indicate that v-src did not su ce for malignant transformation, and that astrocytomas were the result of a multistep process necessitating co-operation of additional genetic events.

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“…Les cellules endoth61iales poss6dent un syst6me sp6cifique pour le transport de la leucine [2]. Holash et al [13] ont montr6 que les cellules endoth61iales sont aussi 6quip6es d'un syst6me de transport pour le glucose (GLUT-l) et la glycoprot6ine P, produit du g6ne de multi-r6sistance aux m6dicaments, deux prot6ines que l'on croyait sp6cifiques des cellules endoth61iales du cerveau. Les souris d6fi-cientes en P-glycoproteine accumulent certains m6dicaments dans leurs testicules [33], et les testicules des souris qui manquent la prot6ine apparent6 mrpl, qui se trouve dans les cellules de Sertoli, sont plus sensibles aux d6gats par l'etoposide phosphate [48].…”

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“…Les souris d6fi-cientes en P-glycoproteine accumulent certains m6dicaments dans leurs testicules [33], et les testicules des souris qui manquent la prot6ine apparent6 mrpl, qui se trouve dans les cellules de Sertoli, sont plus sensibles aux d6gats par l'etoposide phosphate [48]. Holash et al [13] ont aussi montr6 que les cellules leydigiennes, qui sont tr6s pr6s des cellules endoth61iales, poss6dent aussi la prot6ine S-100 et l'enzyme glutamine synth6tase qui sont caract6ristiques des astrocytes, cellules du cerveau qui conFerent aux cellules endoth61iales c6r6brales leurs caract6ristiques sp6cifiques. Plus r6cemment, Ad61a'ide, Mounir Ghabriel [communication personnelle] a montr6 que les cellules endoth6-liales du testicule ont aussi l'antig6ne de la barri6re endoth61iale (EBA) que l'on croyait auparavant sp6cifique des cellules endoth6-liales du cerveau [19].…”

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Physiologie de la Barrière Sang-Testicule

Setchell

2001

Androl.

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RI~SUMI~Des p r e u v e s de l'existence d'une barri~re entre la lumi~re des tubes s6minif~res et le sang sont r e p r 6 s e n t 6 e s par: la coloration in6gale des testicules apr6s injection de certains colorants, la distribution des substances radioaetives dans le testicule, la composition des fluides du rete testis et de la lumi~re des tubes, la vitesse de p6n6tration de diff6rentes substances dans ces fluides, et la pr6sence de jonctions sp6cialis6es entre les cellules de Sertoli qui bloquent la p6n6tration du lanthan u m et d'autres marqueurs opaques aux 61ec-trons dans les tubules. Cette barri~re se d6ve-loppe au m o m e n t de la pubert6. Cependant, les cellules endoth61iales du testicule ont des caract6ristiques qui sont retrouv6es dans les cellules endoth61iales du cerveau qui forment la barri~re sang-cerveau. Le tissu p6ritubu-laire poss~de aussi u n syst~me sp6cifique pour le transport de l'ur~e, et ces deux tissus p e u v e n t aussi r~guler l'entr6e des substances dans le testicule. La barri~re reste effective dans certaines circonstances dans lesquelles la spermatogen~se est perturb~e, mais la barri~re est moins effective p e n d a n t la phase de r~gression testiculaire chez les esp~ces reproduction saisonni~re. I1 existe aussi des traitements qui rompent la barri~re en perturbant la spermatogen~se. I1 faut que les spermatogonies inject~es dans le rete passent travers la barri~re Sertolienne pour r~ta-blir la spermatogen~se dans les testicules infertiles, mais les cellules leuc~miques inject~es dans le rete p e u v e n t aussi passer de la lumi~re dans rinterstitium od u n e r~cidive de la maladie peut survenir.Mots Cl~s : Barri~re, transport, testicule, Sertoli, spermatogen~se, leucdmie Les preuves de l'existence d'une barri~re ou de barri~res entre le sang et les tubules s6mini-Feres sont apparues il y a presque cent ans. Un dessin de Goldmann [11] d a t a n t de 1909 repr6-sente un testicule de rat dans lequel on a inject6 de la teinture bleue pyrrol. On peut voir que les tubes s6minif~res ne sont pas color6s, mais le tissu interstitiel montre une forte coloration bleue. Plus r6cemment, il y a eu d'autres 6tudes de la distribution de substances radioactives mesur6e par autoradiographie, et on a dit que quelques unes 6taient exclues des tubes s6miniFeres [37]. On a pu aussi m e s u r e r l'espace ou volume de distribution, que l'on exprime en microlitres par gramme, d'un indicateur radioactif, comme le Cr-EDTA par exemple, espace qui repr6sente n o r m a l e m e n t 60 % du volume du tissu interstitiel quand il est estim6 par morphom6trie [40]. Ce chiffre est augment6 si la barri~re est rompue [41].

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Barrier properties of testis microvessels.

Cited by 122 publications

References 48 publications

Expression of multiple glutamate transporter splice variants in the rodent testis

Expression of multiple glutamate transporter splice variants in the rodent testis

Development and malignant progression of astrocytomas in GFAP-v-src transgenic mice

Physiologie de la Barrière Sang-Testicule

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