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Updated: Mar 31, 2026

Cell Membrane Repair Assay Using a Two-photon Laser Microscope
Published on: January 2, 2018
Calcium signaling in membrane repair
Xiping Cheng1, Xiaoli Zhang1, Lu Yu1
1Department of Molecular, Cellular, and Developmental Biology, University of Michigan, 3089 Natural Science Building (Kraus), 830 North University, Ann Arbor, MI 48109, USA.
Cellular plasma membrane (PM) repair involves calcium (Ca2+) influx and release. This review explores how Ca2+ channels and sensors orchestrate PM resealing after cellular damage.
Area of Science:
- Cell Biology
- Membrane Biology
- Biochemistry
Background:
- Plasma membrane (PM) resealing is a rapid cellular repair process crucial for cell survival following disruptions.
- Existing models of PM repair (lipid-patch, endocytic removal, macro-vesicle shedding) implicate local increases in intracellular calcium (Ca2+) at injury sites.
- Multiple Ca2+ sensors, including synaptotagmin (Syt) VII, dysferlin, and apoptosis-linked gene-2 (ALG-2), are involved, suggesting Ca2+ regulates diverse repair steps.
Purpose of the Study:
- To review the mechanisms of plasma membrane resealing.
- To discuss the role of intracellular Ca2+ stores in PM repair.
- To highlight the function of vesicular Ca2+ channels and Ca2+ sensors in orchestrating membrane repair.
Main Methods:
- Literature review of studies on plasma membrane repair mechanisms.
- Analysis of the role of calcium (Ca2+) in cellular resealing processes.
- Examination of Ca2+ sensors and vesicular channels involved in membrane repair.
Main Results:
- PM resealing relies on local Ca2+ increases at injury sites.
- Both extracellular Ca2+ and intracellular Ca2+ release contribute to PM repair.
- Specific Ca2+ sensors and vesicular channels are recruited to damage sites to facilitate resealing.
Conclusions:
- Plasma membrane repair is a complex process regulated by calcium.
- Multiple Ca2+ sources and sensors coordinate to ensure effective resealing of cellular damage.
- Understanding these mechanisms offers insights into cell survival and repair pathways.
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