Involvement of calmodulin and protein kinase C in the regulation of K+ transport by carbachol across the rat distal colon

Heinke, Bernhard; Ribeiro, Renato Weller; Diener, Martin

doi:10.1016/s0014-2999(99)00416-1

Cited by 15 publications

(15 citation statements)

References 23 publications

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“…Consequently, calcium and PKC are important in Campylobacter jejuni-induced changes in Na + and Cltransport in rat ileum in vitro [36]. CaM and PKC also control K + -transport in rat distal colon [37]. We found that W13 (a specific CaM antagonist) eliminated the LPS effect on Dfructose intestinal uptake, suggesting that calcium, could be an intracellular messenger in the inhibition of sugar intestinal transport via its interaction with calmodulin.…”

Section: Discussionmentioning

confidence: 74%

“…PKC is important in the sensitization of endothelial cells to bacterial endotoxin challenge [36]. PKC has also been related to the transport of electrolytes in rat colon and ileum [35,37] and sodium-glucose, L-arginine and L-alanine transport in different cell lines [39 -42]. In order to elucidate whether PKC was involved in LPS inhibition, staurosporine and GF-109203X were used as PKC inhibitors and PMA as activator.…”

Section: Discussionmentioning

confidence: 99%

“…3). Likewise, we measured the sugar uptake in the presence of staurosporine and GF-109203X a nonselective and selective protein kinase C (PKC) inhibitor respectively, at 10 -8 , 10 -7 and 10 -6 M [26,27]. The LPS effect disappeared at 10 -7 or 10 -6 M with staurosporine and 10 -6 M with GF-109203X (Tables 3, 4).…”

Section: Cellular Mechanism Of Lps Action On D-fructose Intestinal Abmentioning

confidence: 99%

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Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

García-Herrera

Abad

Rodríguez-Yoldi

2003

Inflammation Research

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Section: Cellular Mechanism Of Lps Action On D-fructose Intestinal Abmentioning

confidence: 99%

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Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

García-Herrera

Abad

Rodríguez-Yoldi

2003

Inflammation Research

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“…For example, trafficking of aquaporin-2 to the apical membrane of collecting duct principal cells in response to vasopressin is dependent on intracellular calcium release from ryanodine-sensitive stores (7). Intracellular calcium also regulates H ϩ -K ϩ -ATPase in both the stomach and the colon (20,26,28,39), 10% CO 2 -dependent stimulation of CCD H ϩ -K ϩ -ATPase (52), and collecting duct H ϩ -ATPase stimulation by metabolic acidosis (38,43). Finally, intracellular calcium plays a role in SNARE-protein-mediated vesicle fusion with plasma membranes (27).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms through which ammonia regulates cortical collecting duct net proton secretion

Frank

Wingo

Andrews

et al. 2002

American Journal of Physiology-Renal Physiology

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Ammonia stimulates cortical collecting duct (CCD) net bicarbonate reabsorption by activating an apical H+-K+-ATPase through mechanisms that are independent of ammonia's known effects on intracellular pH and active sodium transport. The present studies examined whether this stimulation occurs through soluble N-ethylmaleimide-sensitive fusion attachment receptor (SNARE) protein-mediated vesicle fusion. Rabbit CCD segments were studied using in vitro microperfusion, and transepithelial bicarbonate transport was measured using microcalorimetry. Ammonia's stimulation of bicarbonate reabsorption was blocked by either chelating intracellular calcium with 1,2-bis(2-aminophenoxy)ethane- N,N,N',N'-tetraacetic acid acetoxymethyl ester or by inhibiting microtubule polymerization with colchicine compared with parallel studies performed in the absence of these inhibitors. An inactive structural analog of colchicine, lumicolchicine, did not alter ammonia's stimulation of bicarbonate reabsorption. Tetanus toxin, a zinc endopeptidase specific for vesicle-associated SNARE (v-SNARE) proteins, prevented ammonia from stimulating net bicarbonate reabsorption. Consistent with the functional evidence for v-SNARE involvement, antibodies directed against a conserved region of isoforms 1–3 of the tetanus toxin-sensitive, vesicle-associated membrane protein (VAMP) members of v-SNARE proteins labeled the apical and subapical region of collecting duct intercalated cells. Similarly, antibodies to NSF protein, a protein involved in activation of SNARE proteins for subsequent vesicle fusion, localized to the apical and subapical region of collecting duct intercalated cells. These results indicate that ammonia stimulates CCD bicarbonate reabsorption through an intracellular calcium-dependent, microtubule-dependent, and v-SNARE-dependent mechanism that appears to involve insertion of cytoplasmic vesicles into the apical plasma membrane of CCD intercalated cells.

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“…PKC has also been shown to contribute to electrolyte transport regulation in the rat colon and ileum [Kaur et al, 1993;Heinke et al, 1999], and to Dglucose, L-arginine, and L-alanine transport in several cell lines [Delezay et al, 1995;Pan and Stevens, 1995a,b;Vayro and Silverman, 1999]. In COS-7 cells transfected with rabbit SGLT1 cDNA, activation of PKC decreases the V max of SGLT1 with no effect on the number of transporters present at the cell surface, suggesting that PKC may diminish the turnover rate of the transporter [Vayro and Silverman, 1999].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of TNF‐α on the intestinal absorption of galactose

Amador¹,

García-Herrera²,

Marca³

et al. 2006

J of Cellular Biochemistry

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Sepsis is a systemic response to infection in which toxins, such as bacterial lipopolysaccharide (LPS), stimulate the production of inflammatory mediators like the cytokine tumor necrosis factor alpha (TNF-alpha). Previous studies from our laboratory have revealed that LPS inhibits the intestinal absorption of L-leucine and D-fructose in rabbit when it was intravenously administered, and that TNF-alpha seems to mediate this effect on amino acid absorption. To extend this work, the present study was designed to evaluate the possible effect of TNF-alpha on D-galactose intestinal absorption, identify the intracellular mechanisms involved and establish whether this cytokine mediates possible LPS effects. Our findings indicate that TNF-alpha decreases D-galactose absorption both in rabbit intestinal tissue preparations and brush-border membrane vesicles. Western blot analysis revealed reduced amounts of the Na+/glucose cotransporter (SGLT1) protein in the plasma membrane attributable to the cytokine. On the contrary, TNF-alpha increased SGLT1 mRNA levels. Specific inhibitors of the secondary messengers PKC, PKA, the MAP kinases p38 MAP, JNK, MEK1/2 as well as the proteasome, diminished the TNF-alpha-evoked inhibitory effect. LPS inhibition of the uptake of the sugar was blocked by a TNF-alpha antagonist. In conclusion, TNF-alpha inhibits D-galactose intestinal absorption by decreasing the number of SGLT1 molecules at the enterocyte plasma membrane through a mechanism in which several protein-like kinases are involved.

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Involvement of calmodulin and protein kinase C in the regulation of K+ transport by carbachol across the rat distal colon

Cited by 15 publications

References 23 publications

Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

Effect of lipopolysaccharide on D-fructose transport across rabbit jejunum

Mechanisms through which ammonia regulates cortical collecting duct net proton secretion

Inhibitory effect of TNF‐α on the intestinal absorption of galactose

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