The mechanism by which stromal cells fill voids in injured tissue remains a fundamental question in regenerative medicine. While it is well-established that fibroblasts fill voids by depositing extracellular matrix (ECM) proteins as they migrate toward the wound site, little is known about their ability to adopt an epithelial-like purse-string behavior. To investigate fibroblast behavior during gap closure, we created an artificial wound with a large void space. We discovered that fibroblasts could form a free-standing bridge over deep microvoids, closing the void via purse-string contraction, a mechanism previously thought to be unique to epithelial wound closure. The findings also revealed that myosin II mediated contractility and intercellular adherent junctions were required for the closure of the fibroblast gap in our fabricated three-dimensional artificial wound. To fulfill their repair function under the specific microenvironmental conditions of wounds, fibroblasts appeared to acquire the structural features of epithelial cells, namely, contractile actin bundles that span over multiple cells along the boundary. These findings shed light on a novel mechanism by which stromal cells bridge the 3D gap during physiological processes such as morphogenesis and wound healing.
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http://dx.doi.org/10.1021/acsami.2c07952 | DOI Listing |
Exp Neurol
December 2024
Department of Neurology, Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Chuoku, Niigata 951-8585, Japan. Electronic address:
Background: Despite advances in reperfusion therapies, ischemic stroke remains a major cause of long-term disability due to residual hypoxic lesions persisting after macrovascular reperfusion. These residual hypoxic lesions, caused by microvascular dysfunction, represent an important therapeutic target. We previously demonstrated that oxygen-glucose-deprived peripheral blood mononuclear cells (OGD-PBMCs) migrate to ischemic brain regions and promote functional recovery after stroke.
View Article and Find Full Text PDFCancer Lett
December 2024
Department of Hepatobiliary and Pancreatic Surgery, Peking University First Hospital, Beijing 100034, China. Electronic address:
Pancreatic cancer (PC) is one of the most malignant solid cancers, and PC metastasis, particularly liver metastasis, is a major cause of cancer mortality. A key event in tumor metastasis is the formation of pre-metastatic niche (PMN), which provides a microenvironment conducive to tumor cells colonization and progression. Various molecules loaded in tumor-derived exosomes (TDEs) contribute to PMN formation and distant tumor metastasis, by regulating immune and stromal cell function, inducing angiogenesis, and promoting metabolic reprogramming.
View Article and Find Full Text PDFClin Exp Med
December 2024
Department of Pathology, Shenzhen Qianhai Shekou Free Trade Zone Hospital, Shenzhen, 518000, Guangdong, People's Republic of China.
This study aims to comprehensively analyze the role of the exportin (XPO) family in the development and progression of cancer. These nuclear transport proteins have been increasingly recognized for their involvement in oncogenic processes and tumor growth. We utilized updated public databases and bioinformatics tools to assess the expression levels of the XPO family and their associations with key oncological markers including patient survival, immune subtypes, tumor microenvironment, stemness scores, drug sensitivity, and DNA methylation across various cancers.
View Article and Find Full Text PDFJ Transl Med
December 2024
Department of Pancreatic surgery, Huashan Hospital, Fudan University, Shanghai, 200040, China.
Background: The typical pathological feature of pancreatic ductal adenocarcinoma (PDAC) is a significant increase in stromal reaction, leading to a hypoxic and poorly vascularized tumor microenvironment. Tumor cells undergo metabolic reprogramming, such as the Warburg effect, yet the underlying mechanisms are not fully understood.
Methods: Interference and overexpression experiments were conducted to analyze the in vivo and in vitro effects of USP7 on the growth and glycolysis of tumor cells.
Exp Eye Res
December 2024
Harry S. Truman Memorial Veterans' Hospital, Columbia, Missouri, USA; Departments of Veterinary Medicine & Surgery and Biomedical Sciences, University of Missouri, Columbia, Missouri, USA; Mason Eye Institute, School of Medicine, University of Missouri, Columbia, Missouri, USA. Electronic address:
Sulfur mustard gas (SM), an alkylating and vesicating agent, has been used frequently in many wars and conflicts. SM exposure to the eye results in several corneal abnormalities including scar/fibrosis formation. However, molecular mechanism for SM induced corneal fibrosis development is poorly understood.
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