The characteristics of hepatocyte intramitochondrial filaments (IMF's) were studied in 16 patients undergoing jejunal ileal bypass for morbid obesity. At the time of bypass, all of the liver biopsies showed varying degrees of steatosis and IMF's were present in 13 of the 16 operative specimens. The IMF's were most prominent in the periportal cells, whereas the intracellular lipid was concentrated in centrilobular cells. Midzonal hepatocytes were intermediate in both respects. The IMF'S were more abundant in biopsies showing moderate steatosis than in those with marked lipid accumulation in which the IMF's were limited to hepatocytes in juxtaposition to portal triads. The IMF's appeared to originate from mitochondrial cristae. When steatosis resolved 12 to 18 months after intestinal bypass the prevalence of IMF's diminished also. It is hypothesized that the presence of IMF's is ultrastructural evidence of an adaption to an altered metabolic environment which resolves when the inciting influence is removed.
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Hereditary sensory neuropathy type 1A (HSN1A) is an autosomal, dominantly inherited peripheral neuropathy caused by mutations in serine palmitoyl transferase long chain 1 (SPTLC1), involved in the synthesis of sphingolipids. We have previously reported calcium imbalance, as well as mitochondrial and ER stress in both HSN1 patient lymphoblasts and a transiently transfected cell model. In this study, we investigated the role of the Ca-activated protease calpain in destabilizing the cell cytoskeleton, by examining calpain activity in SH-SY5Y cells overexpressing the V144D mutant and changes in microtubule-associated proteins (MAP).
View Article and Find Full Text PDFJ Cell Sci
November 2020
Department of Molecular Biology and Biochemistry, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita 565-0871, Japan
Cells
February 2019
A.N.Belozersky Institute of Physico-Chemical Biology, Moscow State University, Moscow 119991, Russia.
Thirty-five years ago, we described fragmentation of the mitochondrial population in a living cell into small vesicles (mitochondrial fission). Subsequently, this phenomenon has become an object of general interest due to its involvement in the process of oxidative stress-related cell death and having high relevance to the incidence of a pathological phenotype. Tentatively, the key component of mitochondrial fission process is segregation and further asymmetric separation of a mitochondrial body yielding healthy (normally functioning) and impaired (incapable to function in a normal way) organelles with subsequent decomposition and removal of impaired elements through autophagy (mitophagy).
View Article and Find Full Text PDFOncotarget
September 2017
Department of Pathology, Nanfang Hospital and School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China.
Directional migration is a cost-effective movement allowing invasion and metastatic spread of cancer cells. Although migration related to cytoskeletal assembly and microenvironmental chemotaxis has been elucidated, little is known about interaction between extracellular and intracellular molecules for controlling the migrational directionality. A polarized expression of prohibitin (PHB) in the front ends of CRC cells favors metastasis and is correlated with poor prognosis for 545 CRC patients.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
November 2009
Research Program of Molecular Neurology, Institute of Biomedicine, University of Helsinki, FIN-00290 Helsinki, Finland.
LACTB is a mammalian active-site serine protein that has evolved from a bacterial penicillin-binding protein. Penicillin-binding proteins are involved in the metabolism of peptidoglycan, the major bacterial cell wall constituent, implying that LACTB has been endowed with novel biochemical properties during eukaryote evolution. Here we demonstrate that LACTB is localized in the mitochondrial intermembrane space, where it is polymerized into stable filaments with a length extending more than a hundred nanometers.
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