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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Actins, Adenosine Triphosphate, Adult, Biological Transport, Calcium, Cells, Cultured, Cytochalasin D, Cytoskeleton, Humans, Keratinocytes, Middle Aged, Neurofibromatosis 1, Signal Transduction, Skin, Thapsigargin.
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Is an intact actin-containing cytoskeleton required for capacitative calcium entry , but not for ATP-induced calcium-mediated cell signaling in cultured human keratinocytes? Context: The present study was focused on structural relationship between intracellular calcium stores and plasma membrane store-operated calcium channels in cultured normal and NF1 keratinocytes. Calcium mobilization induced by thapsigargin or extracellular ATP was studied in control and cytochalasin D-treated human keratinocytes. Treatment of keratinocytes with cytochalasin D disrupted the actin cytoskeleton and changed the cells from a planar, extended morphology, to a rounded shape. In normal control keratinocytes, thapsigargin induced a marked increase in intracellular calcium concentration ([Ca2+]i). The capacitative calcium influx of cytochalasin D-treated normal keratinocytes was significantly weaker compared to normal control cells. In normal keratinocytes, ATP induced a rapid and transient increase in [Ca2+]i. Thus disruption of the cytoskeleton blocked thapsigargin-induced calcium mobilization, but had no effect on ATP-induced [Ca2+]i mobilization in keratinocytes. The results suggest that microfilaments play crucial role for functional capacitative Ca2+ entry in cultured keratinocytes. The cytoskeleton and calcium mediated cell signaling have been demonstrated to be abnormal in keratinocytes cultured from patients with neurofibromatosis type 1 (NF1). In NF1 keratinocytes, thapsigargin induced a slow and moderate increase in [Ca2+]i. The effect of cytochalasin D on NF1 keratinocytes was less pronounced compared to normal keratinocytes. In NF1 keratinocytes, ATP induced a rapid and transient increase in [Ca2+]i.
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The actin microfilaments play a crucial role for functional capacitative Ca2+ entry in cultured keratinocytes, and that aberrant organization of cytoskeleton may partly explain altered calcium-mediated cell signaling in NF1. Final Decision: yes