scholarly journals The intact parasympathetic nerve promotes submandibular gland regeneration through ductal cell proliferation

2021 ◽  
Author(s):  
Xue Wang ◽  
Zhilin Li ◽  
Qi Shao ◽  
Chunmei Zhang ◽  
Jinsong Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Submandibular Gland ◽  
Parasympathetic Nerve ◽  
Ductal Cell

TAZ inhibits acinar cell differentiation but promotes immature ductal cell proliferation in adult mouse salivary glands

2021 ◽  
Author(s):  
Yosuke Miyachi ◽  
Miki Nishio ◽  
Junji Otani ◽  
Shinji Matsumoto ◽  
Akira Kikuchi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Differentiation ◽  
Salivary Glands ◽  
Acinar Cell ◽  
Adult Mouse ◽  
Ductal Cell

scholarly journals The proportion of periportal mesenchyme to ductal epithelial cells acts as a proliferative rheostat in liver regeneration

2020 ◽  
Author(s):  
Lucía Cordero-Espinoza ◽  
Timo N. Kohler ◽  
Anna M. Dowbaj ◽  
Bernhard Strauss ◽  
Olga Sarlidou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tissue Injury ◽  
Portal Tract ◽  
Mesenchymal Cells ◽  
Dependent Manner ◽  
Cell Contacts ◽  
Ductal Cells ◽  
Ductal Cell ◽  
Cell Cell

AbstractIn the homeostatic liver, ductal cells intermingle with a microenvironment of endothelial and mesenchymal cells to form the functional unit of the portal tract. Ductal cells proliferate rarely in homeostasis but do so transiently after tissue injury to replenish any lost epithelium. We have shown that liver ductal cells can be expanded as liver organoids that recapitulate several of the cell-autonomous mechanisms of regeneration, but lack the stromal cell milieu of the biliary tract in vivo. Here, we describe a subpopulation of SCA1+ periportal mesenchymal cells that closely surrounds ductal cells in vivo and exerts a dual control on their proliferative capacity. Mesenchymal-secreted mitogens support liver organoid formation and expansion from differentiated ductal cells. However, direct mesenchymal-to-ductal cell-cell contact, established following a microfluidic co-encapsulation that enables the cells to self-organize into chimeric organoid structures, abolishes ductal cell proliferation in a mesenchyme-dose dependent manner. We found that it is the ratio between mesenchymal and epithelial cell contacts that determines the net outcome of ductal cell proliferation both in vitro, and in vivo, during damage-regeneration. SCA1+ mesenchymal cells control ductal cell proliferation dynamics by a mechanism involving, at least in part, Notch signalling activation. Our findings underscore how the relative abundance of cell-cell contacts between the epithelium and its mesenchymal microenvironment are key regulatory cues involved in the control of tissue regeneration.SummaryIn the homeostatic liver, the ductal epithelium intermingles with a microenvironment of stromal cells to form the functional unit of the portal tract. Ductal cells proliferate rarely in homeostasis but do so transiently after tissue injury. We have shown that these cells can be expanded as liver organoids that recapitulate several of the cell-autonomous mechanisms of regeneration, but lack the stromal cell milieu of the portal tract in vivo. Here, we describe a subpopulation of SCA1+ periportal mesenchymal niche cells that closely surrounds ductal cells in vivo and exerts a dual control on their proliferative capacity. Mesenchymal-secreted mitogens support liver organoid formation and expansion from differentiated ductal cells. However, direct mesenchymal-to-ductal cell-cell contact, established through a microfluidic co-encapsulation method that enables the cells to self-organize into chimeric organoid structures, abolishes ductal cell proliferation in a mesenchyme-dose dependent manner. We found that it is the ratio between mesenchymal and epithelial cell contacts that determines the net outcome of ductal cell proliferation both in vitro, and in vivo, during damage-regeneration. SCA1+ mesenchymal cells control ductal cell proliferation dynamics by a mechanism involving, at least in part, Notch signalling activation. Our findings re-evaluate the concept of the cellular niche, whereby the proportions of cell-cell contacts between the epithelium and its mesenchymal niche, and not the absolute cell numbers, are the key regulatory cues involved in the control of tissue regeneration.

Salivary Growth Factors in Health and Disease

2000 ◽  
Vol 14 (1) ◽  
pp. 99-102 ◽  
Author(s):  
H. Kagami ◽  
Y. Hiramatsu ◽  
S. Hishida ◽  
Y. Okazaki ◽  
K. Horie ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Salivary Gland ◽  
Growth Factors ◽  
Growth Factor ◽  
Submandibular Gland ◽  
Cultured Cells ◽  
Healing Process ◽  
Physiological Role ◽  
Gland Cells ◽  
Salivary Gland Cells

The salivary gland is considered to be a reservoir of many growth factors in rodents. In humans, the epidermal growth factor, basic fibroblast growth factor, and insulin and insulin-like growth factor family have also been detected in this gland, but their physiological role remains unclear. In this study, we focused on bFGF, which is a well-known mitogen for various types of cells, and is present in the salivary gland as well as in saliva. The roles of bFGF in the salivary gland were investigated by three different procedures. First, the effects of bFGF on the salivary gland cells were investigated with a monolayer culture of normal submandibular gland cells. The effects of different concentrations of bFGF on the second passage of these cultured cells were examined. In both human and rat cultured submandibular gland cells, bFGF accelerated the cell proliferation at a concentraion of 100 ng/mL or higher. Next, an atrophic model of the rat submandibular gland was used to examine the ability of bFGF to accelerate tissue repair. Two weeks after ductal ligation, the ligature was removed, and various amounts of bFGF, isoproterenol, or saline were administered via a retrograde duct instillation. Both isoproterenol and bFGF increased acinar and ductal cell proliferation significantly. To determine the role of bFGF in saliva, we investigated its effect on the healing process of oral mucosal defects. Four-millimeter mucosal defects were made to the depth of the periosteum in the rat palate under anesthesia. bFGF or vehicle alone was applied once only at the time of surgery as a suspension. At days 3, 5, and 7 in the bFGF group, significant increases in the degree of re-epithelialization were found in treated groups. These results indicate that its action as a mitogen stimulus is the major effect of bFGF on salivary gland cells and mucosal epithelium.

Upregulation of the expression of Fas antigen and Fas ligand in a human submandibular gland ductal cell line by okadaic acid

2000 ◽  
Vol 45 (8) ◽  
pp. 657-666 ◽  
Author(s):  
Yasuhiro Morimoto ◽  
Hiroyuki Morimoto ◽  
Hirohiko Okamura ◽  
Kimiko Nomiyama ◽  
Nobuaki Nakamuta ◽  
...  
Keyword(s):  
Cell Line ◽  
Submandibular Gland ◽  
Okadaic Acid ◽  
Fas Ligand ◽  
Fas Antigen ◽  
Ductal Cell
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