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Transient decrease in gap junction expression during compensatory renal growth in mice.

Abstract

OBJECTIVES: To examine gap junction expression during compensatory renal growth. Compensatory renal growth is a normal response to the removal of renal cells. Gap junctional intercellular communication plays important roles in homeostatic regulation, differentiation, and synchronization of cellular electronic and metabolic functions. METHODS: The right ureters of 5-week-old ddy mice were dorsally incised and unilaterally obstructed, and the animals were killed at varying intervals. The control group underwent a sham operation. Freeze-fractured kidney tissue samples were studied using electron microscopy. The amount of proliferative cell nuclear antigen-positive cells and connexin 43 (Cx43) protein was studied by immunohistochemistry and Western blotting, respectively. RESULTS: Proliferative cell nuclear antigen-positive cells in the renal tubules increased on days 1 and 2 after surgery that obstructed the ureter, and decreased to normal levels by day 14. The number of gap junctions significantly decreased on days 1 and 2, and then gradually increased to normal levels from days 3 to 14 after surgery. The amount of Cx43 protein in the renal tubules decreased until day 2 and recovered to the same level as that of the control by day 14 after surgery. Significantly, a hyperphosphorylated band of Cx43 in the control kidney was not detected in the operated kidney. CONCLUSIONS: These data suggest that the gap junctional intercellular communication of renal tubular cells during compensatory renal growth after unilateral ureteral obstruction could be temporarily reduced concomitant with a decrease of the expression of a phosphorylated Cx43 protein in renal cortical tubular cells after unilateral ureteral obstruction of the contralateral kidney.

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BibTeXRIS

Shengwen Li, Koichiro Nomata, Tomayoshi Hayashi, Mitsuru Noguchi, Shigeru Kanda, Hiroshi Kanetake. 2002. Transient decrease in gap junction expression during compensatory renal growth in mice.. https://doi.org/10.1016/s0090-4295(02)01837-x

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