Hyaluronan-associated adhesive cues control fiber segregation in the hippocampus

Development ◽  
2001 ◽  
Vol 128 (15) ◽  
pp. 3029-3039
Author(s):  
Eckart Förster ◽  
Shanting Zhao ◽  
Michael Frotscher

In various brain regions, particularly in the hippocampus, afferent fiber projections terminate in specific layers. Little is known about the molecular cues governing this laminar specificity. To this end we have recently shown that the innervation pattern of entorhinal fibers to the hippocampus is mimicked by the lamina-specific adhesion of entorhinal cells on living hippocampal slices, suggesting a role of adhesion molecules in the positioning of entorhinal fibers. Here, we have analyzed the role of extracellular matrix components in mediating this lamina-specific adhesion. We show that hyaluronidase treatment of hippocampal slices abolishes lamina-specific adhesion as well as layer-specific growth of entorhinal fibers to the dentate outer molecular layer in organotypic slice cultures. We conclude that hyaluronan-associated molecules play a crucial role in the formation of the lamina-specific entorhinal projection to the hippocampus.

Bone ◽  
2021 ◽  
Vol 153 ◽  
pp. 116172
Author(s):  
Qin Shengnan ◽  
Samuel Bennett ◽  
Wang Wen ◽  
Li Aiguo ◽  
Xu Jiake

2004 ◽  
Vol 30 (4) ◽  
pp. 609-610
Author(s):  
Shirley Campbell ◽  
Mélissa Otis ◽  
Nicole Gallo‐Payet ◽  
Marcel Daniel Payet

Author(s):  
Zaira Heredia‐Ponce ◽  
José Antonio Gutiérrez‐Barranquero ◽  
Gabriela Purtschert‐Montenegro ◽  
Leo Eberl ◽  
Antonio de Vicente ◽  
...  

2020 ◽  
Vol 20 (3) ◽  
pp. 168-186 ◽  
Author(s):  
Tabinda Urooj ◽  
Bushra Wasim ◽  
Shamim Mushtaq ◽  
Syed Nudrat Nawaid Shah ◽  
Muzna Shah

: In Breast cancer, Lung is the second most common site of metastasis after the bone. Various factors are responsible for Lung metastasis occurring secondary to Breast cancer. Cancer cellderived secretory factors are commonly known as ‘Cancer Secretomes’. They exhibit a prompt role in the mechanism of Breast cancer lung metastasis. They are also major constituents of hostassociated tumor microenvironment. Through cross-talk between cancer cells and the extracellular matrix components, cancer cell-derived extracellular matrix components (CCECs) such as hyaluronan, collagens, laminin and fibronectin cause ECM remodeling at the primary site (breast) of cancer. However, at the secondary site (lung), tenascin C, periostin and lysyl oxidase, along with pro-metastatic molecules Coco and GALNT14, contribute to the formation of pre-metastatic niche (PMN) by promoting ECM remodeling and lung metastatic cells colonization. Cancer cell-derived secretory factors by inducing cancer cell proliferation at the primary site, their invasion through the tissues and vessels and early colonization of metastatic cells in the PMN, potentiate the mechanism of Lung metastasis in Breast cancer. : On the basis of biochemical structure, these secretory factors are broadly classified into proteins and non-proteins. This is the first review that has highlighted the role of cancer cell-derived secretory factors in Breast cancer Lung metastasis (BCLM). It also enumerates various researches that have been conducted to date in breast cancer cell lines and animal models that depict the prompt role of various types of cancer cell-derived secretory factors involved in the process of Breast cancer lung metastasis. In the future, by therapeutically targeting these cancer driven molecules, this specific type of organ-tropic metastasis in breast cancer can be successfully treated.


2006 ◽  
Vol 28 (8) ◽  
pp. 794-801 ◽  
Author(s):  
Renato Donzelli ◽  
Francesco Maiuri ◽  
Gennaro Andrea Piscopo ◽  
Matteo de Notaris ◽  
Andrea Colella ◽  
...  

2017 ◽  
Vol 312 (3) ◽  
pp. F516-F532 ◽  
Author(s):  
Sandhya Xavier ◽  
Ranjit K. Sahu ◽  
Susan G. Landes ◽  
Jing Yu ◽  
Ronald P. Taylor ◽  
...  

We have examined the pathogenic role of increased complement expression and activation during kidney fibrosis. Here, we show that PDGFRβ-positive pericytes isolated from mice subjected to obstructive or folic acid injury secrete C1q. This was associated with increased production of proinflammatory cytokines, extracellular matrix components, collagens, and increased Wnt3a-mediated activation of Wnt/β-catenin signaling, which are hallmarks of myofibroblast activation. Real-time PCR, immunoblots, immunohistochemistry, and flow cytometry analysis performed in whole kidney tissue confirmed increased expression of C1q, C1r, and C1s as well as complement activation, which is measured as increased synthesis of C3 fragments predominantly in the interstitial compartment. Flow studies localized increased C1q expression to PDGFRβ-positive pericytes as well as to CD45-positive cells. Although deletion of C1qA did not prevent kidney fibrosis, global deletion of C3 reduced macrophage infiltration, reduced synthesis of C3 fragments, and reduced fibrosis. Clodronate mediated depletion of CD11bF4/80 high macrophages in UUO mice also reduced complement gene expression and reduced fibrosis. Our studies demonstrate local synthesis of complement by both PDGFRβ-positive pericytes and CD45-positive cells in kidney fibrosis. Inhibition of complement activation represents a novel therapeutic target to ameliorate fibrosis and progression of chronic kidney disease.


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