The aim of this study was to determine the effects of altered ganglioside composition on the expression of Cx37, Cx40, Cx43, Cx45, and Panx1 in different kidney regions of gene knockout mice ( KO) lacking the GD3 synthase enzyme. Experiments were performed in twelve male 6-month-old mice: four wild-type (C57BL/6-type, WT) and eight KO mice. After euthanasia, kidney tissue was harvested, embedded in paraffin wax, and processed for immunohistochemistry. The expression of connexins and Panx1 was determined in different regions of the kidney: cortex (CTX.), outer stripe of outer medulla (O.S.), inner stripe of outer medulla (IN.S.), and inner medulla (IN.MED.). We determined significantly lower expression of Cx37, Cx40, Cx45, and Panx1 in different parts of the kidneys of KO mice compared with WT. The most consistent decrease was found in the O.S. where all markers (Cx 37, 40, 45 and Panx1) were disrupted in St8si1 KO mice. In the CTX. region, we observed decrease in the expression of Cx37, Cx45, and Panx1, while reduced expression of Cx37 and Panx1 was more specific to IN.S. The results of the present study suggest that deficiency of GD3 synthase in KO mice leads to disruption of renal Cx expression, which is probably related to alteration of ganglioside composition.
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http://dx.doi.org/10.3390/ijms23116237 | DOI Listing |
Elife
January 2025
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
The establishment and growth of the arterial endothelium requires the coordinated expression of numerous genes. However, regulation of this process is not yet fully understood. Here, we combined analysis with transgenic mice and zebrafish models to characterize arterial-specific enhancers associated with eight key arterial identity genes (/, , and .
View Article and Find Full Text PDFZygote
December 2024
Department of Embryology, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
Treatment with follicle-stimulating hormone (FSH) and testosterone (T2) and their combination have been observed to be influential on ovarian follicles of 1-day-old mice ovaries cultured for 8 days. Given that extension of the culture period could positively impact the development of follicles in cultured ovaries, the present study was conducted to evaluate the main and interaction effects of FSH by T2 on the development of ovarian follicles in 1-day-old mice ovaries cultured for 12 days. One-day-old mice ovaries were initially cultured with base medium for 4 days; thereafter, different hormonal treatments were added to the culture media, and the culture was continued for 8 additional days until day 12.
View Article and Find Full Text PDFBiol Res
December 2024
Centro de Biología Celular y Biomedicina CEBICEM, Facultad de Medicina y Ciencia, Universidad San Sebastián, Lota 2465, Providencia., Santiago, 7510156, Chile.
Connexins (Cxs) have the ability to form channels that allow the exchange of ions/metabolites between adjacent cells (gap junction channels, GJC) or between the intra- and extra-cellular compartments (hemichannels, HC). Cxs were initially classified as tumor suppressors. However, more recently, it has been shown that Cxs exert anti- and pro-tumorigenic effects depending on the cell and tissue context.
View Article and Find Full Text PDFMol Cell Endocrinol
February 2025
Shanghai-MOST Key Laboratory of Health and Disease Genomics, NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Clinical Medical School, Fudan University, Shanghai, China. Electronic address:
Research Question: Ubiquitin C-terminal hydrolase L1 (UCHL1) is a deubiquitinating enzyme specifically highly expressed in the brain and gonads. Inhibition of UCHL1 hydrolase activity impairs oocyte maturation. Uchl1 knockout mice exhibit reproductive dysfunction, but the underlying pathogenesis remains unclear.
View Article and Find Full Text PDFF S Sci
May 2024
Department of Animal Science, University of California Davis, Davis, California. Electronic address:
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