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TIMP-2 Promotes Wound Healing by Suppressing Matrix Metalloproteinases and Inflammatory Cytokines in Corneal Epithelial Cells.
Am J Pathol
December 2024
Schepens Eye Research Institute of Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA. Electronic address:
Tissue inhibitors of metalloproteinases (TIMPs) modulate extracellular matrix (ECM) remodeling for maintaining homeostasis and promoting cell migration and proliferation. Pathological conditions can alter TIMP homeostasis and aggravate disease progression. The roles of TIMPs have been studied in tissue-related disorders; however, their contributions to tissue repair during corneal injury are undefined.
View Article and Find Full Text PDFNovel peptide inhibitor of matrix Metalloproteinases-1 from pufferfish skin collagen hydrolysates and its potential Photoprotective activity via the MAPK/AP-1 signaling pathway.
J Photochem Photobiol B
December 2024
Fisheries Research Institute of Fujian, National Research and Development Center for Marine Fish Processing, Key Laboratory of Cultivation and High-value Utilization of Marine Organisms in Fujian Province, Xiamen, China. Electronic address:
Takifugu bimaculatus, a pufferfish species farmed in Fujian Province, is known for its non-toxic flesh and collagen-rich skin. We identified a novel collagen-derived matrix metalloproteinase 1 (MMP-1) inhibitory peptide, from T. bimaculatus skin with potent anti-photoaging properties.
View Article and Find Full Text PDFSelf-Adaptive Nanocarriers Overcome Multiple Physiological Barriers to Boosting Chemotherapy of Orthotopic Pancreatic Cancer.
ACS Nano
December 2024
School of Biomedical Sciences and Engineering, Guangzhou International Campus, South China University of Technology, Guangzhou 511442, P. R. China.
Chemotherapy is the primary treatment option for pancreatic cancer, although nanocarrier-based drug delivery systems often struggle with multiple physiological barriers, limiting their therapeutic efficacy. Here, we developed a pH/reactive oxygen species (ROS) dual-sensitive self-adaptive nanocarrier (DAT) encapsulating camptothecin (CPT), an analog of the pancreatic chemotherapeutic drug irinotecan (CPT-11), to enhance chemotherapy outcomes in orthotopic pancreatic cancer by addressing multiple physiological barriers. The nanocarrier features a peripherally positively charged arginine (Arg) residue on DAT and is masked with an acid-labile 2,3-dimethylmaleic anhydride (DA) to improve circulation time.
View Article and Find Full Text PDFLoss of hepatocyte growth factor activator inhibitor type 1 (HAI-1) upregulates MMP-9 expression and induces degradation of the epidermal basement membrane.
Hum Cell
December 2024
Section of Oncopathology and Morphological Pathology, Department of Pathology, Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miazaki, 889-1692, Japan.
Hepatocyte growth factor activator inhibitor type 1 (HAI-1), which is encoded by the SPINT1 gene, is a membrane-associated serine proteinase inhibitor abundantly expressed in epithelial tissues. We had previously demonstrated that HAI-1 is critical for placental development, epidermal keratinization, and maintenance of keratinocyte morphology by regulating cognate proteases, matriptase and prostasin. After performing ultrastructural analysis of Spint1-deleted skin tissues, our results showed that Spint1-deleted epidermis exhibited partially disrupted epidermal basement-membrane structures.
View Article and Find Full Text PDFAssociation of plasma BDNF and MMP-9 levels with mild cognitive impairment: a matched case-control study.
Sci Rep
December 2024
Department of Public Health, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
The prevalence of Alzheimer's disease (AD) is on the rise globally, and everyone who develops AD eventually experiences mild cognitive impairment (MCI) first. Timely intervention at an early stage of the disease may mitigate disease progression. Recent studies indicate that BDNF and MMP-9 play a significant role in the pathogenesis of AD.
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