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  • Title: Effect of Protriptyline on [Ca²⁺]i and Viability in MDCK Renal Tubular Cells.
    Author: Cheng HH, Chou CT, Liang WZ, Kuo CC, Shieh P, Wang JL, Jan CR.
    Journal: Chin J Physiol; 2017 Apr 30; 60(2):114-123. PubMed ID: 28468029.
    Abstract:
    Protriptyline has been used as an antidepressant. Clinically it has been prescribed in the auxiliary treatment of cancer patients. However, its effect on Ca²⁺ signaling and related physiology is unknown in renal cells. This study examined the effect of protriptyline on cytosolic free Ca²⁺ concentrations ([Ca²⁺]i) and viability in Madin-Darby canine kidney (MDCK) tubular cells. Protriptyline induced [Ca²⁺]i rises concentration-dependently. The response was reduced by 20% by removing extracellular Ca²⁺. Protriptyline-induced Ca²⁺ entry was not altered by protein kinase C (PKC) activity but was inhibited by 20% by three modulators of store-operated Ca²⁺ channels: nifedipine, econazole and SKF96365. In Ca²⁺-free medium, treatment with the endoplasmic reticulum Ca²⁺ pump inhibitor 2,5- di-tert-butylhydroquinone (BHQ) or thapsigargin partially inhibited protriptyline-evoked [Ca²⁺]i rises. Conversely, treatment with protriptyline inhibited partially BHQ or thapsigargin-evoked [Ca²⁺]i rises. Inhibition of phospholipase C (PLC) with U73122 did not change protriptyline-induced [Ca²⁺]i rises. Protriptyline at 5-200 μM decreased cell viability, which was not reversed by pretreatment with the Ca²⁺ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid-acetoxymethyl ester (BAPTA/ AM). Together, in MDCK cells, protriptyline induced [Ca²⁺]i rises by evoking PLC-independent Ca²⁺ release from the endoplasmic reticulum and other unknown stores, and Ca²⁺ entry via PKCinsensitive store-operated Ca²⁺ entry. Protriptyline also caused Ca²⁺-independent cell death.
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