scholarly journals Dysferlin regulates cell membrane repair by facilitating injury-triggered acid sphingomyelinase secretion

2014 ◽  
Vol 5 (6) ◽  
pp. e1306-e1306 ◽  
Author(s):  
A Defour ◽  
J H Van der Meulen ◽  
R Bhat ◽  
A Bigot ◽  
R Bashir ◽  
...  
2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Luana L. Scheffer ◽  
Sen Chandra Sreetama ◽  
Nimisha Sharma ◽  
Sushma Medikayala ◽  
Kristy J. Brown ◽  
...  

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaofei Cong ◽  
Nagaraja Nagre ◽  
Jeremy Herrera ◽  
Andrew C. Pearson ◽  
Ian Pepper ◽  
...  

2015 ◽  
Vol 290 (40) ◽  
pp. 24592-24603 ◽  
Author(s):  
Haichang Li ◽  
Pu Duann ◽  
Pei-Hui Lin ◽  
Li Zhao ◽  
Zhaobo Fan ◽  
...  

2010 ◽  
Vol 189 (6) ◽  
pp. 1027-1038 ◽  
Author(s):  
Christina Tam ◽  
Vincent Idone ◽  
Cecilia Devlin ◽  
Maria Cecilia Fernandes ◽  
Andrew Flannery ◽  
...  

Rapid plasma membrane resealing is essential for cellular survival. Earlier studies showed that plasma membrane repair requires Ca2+-dependent exocytosis of lysosomes and a rapid form of endocytosis that removes membrane lesions. However, the functional relationship between lysosomal exocytosis and the rapid endocytosis that follows membrane injury is unknown. In this study, we show that the lysosomal enzyme acid sphingomyelinase (ASM) is released extracellularly when cells are wounded in the presence of Ca2+. ASM-deficient cells, including human cells from Niemann-Pick type A (NPA) patients, undergo lysosomal exocytosis after wounding but are defective in injury-dependent endocytosis and plasma membrane repair. Exogenously added recombinant human ASM restores endocytosis and resealing in ASM-depleted cells, suggesting that conversion of plasma membrane sphingomyelin to ceramide by this lysosomal enzyme promotes lesion internalization. These findings reveal a molecular mechanism for restoration of plasma membrane integrity through exocytosis of lysosomes and identify defective plasma membrane repair as a possible component of the severe pathology observed in NPA patients.


2009 ◽  
Vol 96 (3) ◽  
pp. 361a ◽  
Author(s):  
Chuanxi Cai ◽  
Haruko Masumiya ◽  
Noah Weisleder ◽  
Noriyuki Matsuda ◽  
Miyuki Nishi ◽  
...  

2000 ◽  
Vol 11 (12) ◽  
pp. 4339-4346 ◽  
Author(s):  
Tatsuru Togo ◽  
Tatiana B. Krasieva ◽  
Richard A. Steinhardt

We hypothesized that the requirement for Ca2+-dependent exocytosis in cell-membrane repair is to provide an adequate lowering of membrane tension to permit membrane resealing. We used laser tweezers to form membrane tethers and measured the force of those tethers to estimate the membrane tension of Swiss 3T3 fibroblasts after membrane disruption and during resealing. These measurements show that, for fibroblasts wounded in normal Ca2+ Ringer's solution, the membrane tension decreased dramatically after the wounding and resealing coincided with a decrease of ∼60% of control tether force values. However, the tension did not decrease if cells were wounded in a low Ca2+ Ringer's solution that inhibited both membrane resealing and exocytosis. When cells were wounded twice in normal Ca2+ Ringer's solution, decreases in tension at the second wound were 2.3 times faster than at the first wound, correlating well with twofold faster resealing rates for repeated wounds. The facilitated resealing to a second wound requires a new vesicle pool, which is generated via a protein kinase C (PKC)-dependent and brefeldin A (BFA)-sensitive process. Tension decrease at the second wound was slowed or inhibited by PKC inhibitor or BFA. Lowering membrane tension by cytochalasin D treatment could substitute for exocytosis and could restore membrane resealing in low Ca2+ Ringer's solution.


2015 ◽  
Vol 108 (2) ◽  
pp. 612a
Author(s):  
Hanley Ma ◽  
Jason Liu ◽  
Zehua Bian ◽  
Yuqi Cui ◽  
Xinyu Zhou ◽  
...  

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