Cx30.2 deletion causes imbalances in testicular Cx43, Cx46, and Cx50 and insulin receptors. Reciprocally, diabetes/obesity alters Cx30.2 in mouse testis
Cx30.2 protein content and localization were assessed during development. An account of Cx30.2, Cx43, Cx46, and Cx50, and insulin receptor (IR) responses to , , or deficiency in mouse interstitial tissue (ITf)- and seminiferous tubule-enriched fractions (STf) is given. The impact of high glucose/ins...
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Published in | American journal of physiology. Regulatory, integrative and comparative physiology Vol. 318; no. 6; pp. R1078 - R1090 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Physiological Society
01.06.2020
|
Series | Hormones, Reproduction and Development |
Subjects | |
Online Access | Get full text |
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Summary: | Cx30.2 protein content and localization were assessed during development. An account of Cx30.2, Cx43, Cx46, and Cx50, and insulin receptor (IR) responses to
,
, or
deficiency in mouse interstitial tissue (ITf)- and seminiferous tubule-enriched fractions (STf) is given. The impact of high glucose/insulin on Cx30.2 was investigated in spontaneously diabetic and obese
and
mouse testis and anterior pituitary (AP). Cx30.2 labeled contacts in vascular endothelial and Leydig cells and Sertoli cell junctions in stage V-VII. Cx30.2 expression is regulated differently in the interstitium and tubules. Cx30.2 at 30-kDa levels peaked by 28 days in ITf and by 14 days in STf. In STf, deleting
decreased Cx43 and Cx50, whereas deleting
downregulated Cx30.2. The opposite occurred in ITf. In STf, deleting
upregulated Cx46 except the full-length reciprocally, deleting
upregulated Cx30.2. In ITf,
deficiency upregulated full-length and phosphorylated Cx46, whereas deleting
downregulated 48- to 50-kDa Cx30.2. The
and
mouse ITf, STf, and AP showed imbalanced Cx30.2 levels. IRα levels at 135 kDa declined in
and
mouse ITf and
and Cx50-/- STf. IRβ at 98 to 110 kDa dropped in
and
mice STf suggesting that
deficiency decreases active IR sites. The results show the connexins interdependence and interaction and that altering a single connexin changes the remaining connexins expression, which can modify gap junction-mediated glucose exchanges in contacting cells. Data suggest that glucose/insulin influences Cx30.2 turnover in testis and AP and, reciprocally, that connexins modulate testis glucose uptake and response to insulin. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0363-6119 1522-1490 |
DOI: | 10.1152/ajpregu.00044.2020 |