Connexin 30.2 is expressed in exocrine vascular endothelial and ductal epithelial cells throughout pancreatic postnatal development

Coronel-Cruz, Cristina; Sánchez, I. H.; Hernández-Téllez, Beatriz; Rodríguez‐Mata, Verónica; Pinzón-Estrada, Enrique; Castell-Rodrı́guez, Andrés; Pérez-Armendáriz, E. Martha

doi:10.1016/j.acthis.2018.06.007

Cited by 2 publications

(1 citation statement)

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“…Cx30.2 was said to be expressed in the interstitial tissue of the mouse testis (39). Cx30.2 is expressed in pancreatic ␤ cells and vascular endothelial cells of the islet of the mouse pancreas (8) as well as in the vascular endothelial and ductal epithelial cells of the exocrine mouse pancreas (9).…”

Section: Introductionmentioning

confidence: 99%

Cx30.2 deletion causes imbalances in testicular Cx43, Cx46, and Cx50 and insulin receptors. Reciprocally, diabetes/obesity alters Cx30.2 in mouse testis

Pelletier

Layeghkhavidaki

Kumar

et al. 2020

American Journal of Physiology-Regulatory, Integrative and Comp

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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 Cx30.2, Cx46, or Cx50 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 db/db and ob/ob 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 Cx30.2 decreased Cx43 and Cx50, whereas deleting Cx50 downregulated Cx30.2. The opposite occurred in ITf. In STf, deleting Cx30.2 upregulated Cx46 except the full-length reciprocally, deleting Cx46 upregulated Cx30.2. In ITf, Cx30.2 deficiency upregulated full-length and phosphorylated Cx46, whereas deleting Cx46 downregulated 48- to 50-kDa Cx30.2. The db/db and ob/ob mouse ITf, STf, and AP showed imbalanced Cx30.2 levels. IRα levels at 135 kDa declined in Cx30.2−/− and Cx50−/− mouse ITf and Cx46−/− and Cx50−/− STf. IRβ at 98 to 110 kDa dropped in Cx30.2−/− and Cx46−/− mice STf suggesting that Cx30.2 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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Section: Introductionmentioning

confidence: 99%