L-type voltage-operated Ca+2 channels modulate transient Ca +2 influx triggered by activation of sertoli cell surface L-selectin

Tzu Jen Kao, Clarke F. Millette

研究成果: 雜誌貢獻文章

4 引文 (Scopus)

摘要

Near the base of mammalian seminiferous epithelium, Sertoli cells are joined by tight junctions, which constitute the blood-testis barrier. Differentiating germ cells are completely enveloped by Sertoli cells and must traverse the tight junctions during spermatogenic cycle. Fol lowing the specific ligand activation of L-selectin, the up-regulated Rho family small G-proteins have been implicated as important modulators of tight junctional dynamics. Although the activation of L-selectin transmits subsequent intracellular signals in a Ca+2-dependent fashion in various cell types, little is understood regarding the signaling pathways utilized by L-selectin in Sertoli cells. Therefore, we have examined the possible resultant calcium influx triggered by specific ligand-activation of cell surface L-selectin receptors or by cross-linking of L-selectin with anti-L-selectin. Spectrofluorimetric studies demonstrate increase of intracellular Ca+2 levels immediately after the treatment of the L-selectin ligands, fucoidan and sialyl Lewis-a, or after treatment with anti-L-selectin antibody. We then determined the mechanism of Ca+2 influx by investigating L- and T-type voltage-operated Ca +2 channels, which have been suggested to present in the membranes of Sertoli cells. Data demonstrate that Sertoli cells treated with L-type voltage-operated Ca+2 channel antagonists, nifedipine, diltiazem, or verapamil, lead to dose-dependent blockage of L-selectin-induced Ca+2 influx. Cells treated with mibedradil, a T-type voltage-operated Ca +2 channel antagonist, results in little or no blocking effect. Therefore, we conclude that activation of Sertoli cell L-selectin induces Ca+2 influx, which is at least partially regulated by L-type voltage-operated Ca+2 channels.
原文英語
頁(從 - 到)1023-1037
頁數15
期刊Journal of Cellular Biochemistry
101
發行號4
DOIs
出版狀態已發佈 - 七月 1 2007
對外發佈Yes

指紋

L-Selectin
Sertoli Cells
Chemical activation
Electric potential
Tight Junctions
Ligands
Blood-Testis Barrier
Seminiferous Epithelium
Monomeric GTP-Binding Proteins
Diltiazem
Nifedipine
Verapamil
Germ Cells
Modulators
Blood
Cells
Calcium
Membranes

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

引用此文

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title = "L-type voltage-operated Ca+2 channels modulate transient Ca +2 influx triggered by activation of sertoli cell surface L-selectin",
abstract = "Near the base of mammalian seminiferous epithelium, Sertoli cells are joined by tight junctions, which constitute the blood-testis barrier. Differentiating germ cells are completely enveloped by Sertoli cells and must traverse the tight junctions during spermatogenic cycle. Fol lowing the specific ligand activation of L-selectin, the up-regulated Rho family small G-proteins have been implicated as important modulators of tight junctional dynamics. Although the activation of L-selectin transmits subsequent intracellular signals in a Ca+2-dependent fashion in various cell types, little is understood regarding the signaling pathways utilized by L-selectin in Sertoli cells. Therefore, we have examined the possible resultant calcium influx triggered by specific ligand-activation of cell surface L-selectin receptors or by cross-linking of L-selectin with anti-L-selectin. Spectrofluorimetric studies demonstrate increase of intracellular Ca+2 levels immediately after the treatment of the L-selectin ligands, fucoidan and sialyl Lewis-a, or after treatment with anti-L-selectin antibody. We then determined the mechanism of Ca+2 influx by investigating L- and T-type voltage-operated Ca +2 channels, which have been suggested to present in the membranes of Sertoli cells. Data demonstrate that Sertoli cells treated with L-type voltage-operated Ca+2 channel antagonists, nifedipine, diltiazem, or verapamil, lead to dose-dependent blockage of L-selectin-induced Ca+2 influx. Cells treated with mibedradil, a T-type voltage-operated Ca +2 channel antagonist, results in little or no blocking effect. Therefore, we conclude that activation of Sertoli cell L-selectin induces Ca+2 influx, which is at least partially regulated by L-type voltage-operated Ca+2 channels.",
keywords = "Ca influx, L-selectin, L-type Ca channels, Sertoli cells",
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TY - JOUR

T1 - L-type voltage-operated Ca+2 channels modulate transient Ca +2 influx triggered by activation of sertoli cell surface L-selectin

AU - Kao, Tzu Jen

AU - Millette, Clarke F.

PY - 2007/7/1

Y1 - 2007/7/1

N2 - Near the base of mammalian seminiferous epithelium, Sertoli cells are joined by tight junctions, which constitute the blood-testis barrier. Differentiating germ cells are completely enveloped by Sertoli cells and must traverse the tight junctions during spermatogenic cycle. Fol lowing the specific ligand activation of L-selectin, the up-regulated Rho family small G-proteins have been implicated as important modulators of tight junctional dynamics. Although the activation of L-selectin transmits subsequent intracellular signals in a Ca+2-dependent fashion in various cell types, little is understood regarding the signaling pathways utilized by L-selectin in Sertoli cells. Therefore, we have examined the possible resultant calcium influx triggered by specific ligand-activation of cell surface L-selectin receptors or by cross-linking of L-selectin with anti-L-selectin. Spectrofluorimetric studies demonstrate increase of intracellular Ca+2 levels immediately after the treatment of the L-selectin ligands, fucoidan and sialyl Lewis-a, or after treatment with anti-L-selectin antibody. We then determined the mechanism of Ca+2 influx by investigating L- and T-type voltage-operated Ca +2 channels, which have been suggested to present in the membranes of Sertoli cells. Data demonstrate that Sertoli cells treated with L-type voltage-operated Ca+2 channel antagonists, nifedipine, diltiazem, or verapamil, lead to dose-dependent blockage of L-selectin-induced Ca+2 influx. Cells treated with mibedradil, a T-type voltage-operated Ca +2 channel antagonist, results in little or no blocking effect. Therefore, we conclude that activation of Sertoli cell L-selectin induces Ca+2 influx, which is at least partially regulated by L-type voltage-operated Ca+2 channels.

AB - Near the base of mammalian seminiferous epithelium, Sertoli cells are joined by tight junctions, which constitute the blood-testis barrier. Differentiating germ cells are completely enveloped by Sertoli cells and must traverse the tight junctions during spermatogenic cycle. Fol lowing the specific ligand activation of L-selectin, the up-regulated Rho family small G-proteins have been implicated as important modulators of tight junctional dynamics. Although the activation of L-selectin transmits subsequent intracellular signals in a Ca+2-dependent fashion in various cell types, little is understood regarding the signaling pathways utilized by L-selectin in Sertoli cells. Therefore, we have examined the possible resultant calcium influx triggered by specific ligand-activation of cell surface L-selectin receptors or by cross-linking of L-selectin with anti-L-selectin. Spectrofluorimetric studies demonstrate increase of intracellular Ca+2 levels immediately after the treatment of the L-selectin ligands, fucoidan and sialyl Lewis-a, or after treatment with anti-L-selectin antibody. We then determined the mechanism of Ca+2 influx by investigating L- and T-type voltage-operated Ca +2 channels, which have been suggested to present in the membranes of Sertoli cells. Data demonstrate that Sertoli cells treated with L-type voltage-operated Ca+2 channel antagonists, nifedipine, diltiazem, or verapamil, lead to dose-dependent blockage of L-selectin-induced Ca+2 influx. Cells treated with mibedradil, a T-type voltage-operated Ca +2 channel antagonist, results in little or no blocking effect. Therefore, we conclude that activation of Sertoli cell L-selectin induces Ca+2 influx, which is at least partially regulated by L-type voltage-operated Ca+2 channels.

KW - Ca influx

KW - L-selectin

KW - L-type Ca channels

KW - Sertoli cells

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