Hematopoietic stem cells in wound healing response

Author(s):  
Norifumi Urao ◽  
Jinghua Liu ◽  
Kentaro Takahashi ◽  
Gayathri Ganesh
Author(s):  
Shiri Kuperman ◽  
Ram Efraty ◽  
Ina Arie ◽  
Arkadi Rahmanov ◽  
Marina Rahmanov Gavrielov ◽  
...  

Diabetic wounds’ delayed healing response is still considered a major therapeutic challenge. Stem cells and derived cellular products have been an active field of research for novel therapies referred to as regenerative medicine. It has recently been shown that human oral mucosa stem cells (hOMSCs) are a readily accessible source for obtaining large quantities of stem cells. This study evaluates the potential of mouse oral mucosa stem cells (mOMSCs) to enhance wound healing in a diabetic (db/db) mouse model by morphological and histological analysis. We show that mOMSCs-treated wounds displayed a significantly faster wound-healing response (p ≤ 0.0001), featuring faster re-epithelialization and a larger area of granulation tissue (p ≤ 0.05). Taken together, these results suggest that oral mucosa stem cells might have therapeutic potential in diabetic wound healing.


2020 ◽  
Author(s):  
Yanan Kong ◽  
Liuhanghang Cheng ◽  
Min Xuan ◽  
Hao Ding ◽  
Biao Cheng

Abstract Background Hematopoietic stem cells(HSCs) and mesenchymal stem cells(MSCs) can participate in wound healing. However, very few studies had shown HSCs and MSCs could arrive to the wound and differentiate into tissues. In this study, we intend to investigate the role of bone marrow HSCs and MSCs in wound healing. Methods We first removed the bone marrow of mice by irradiation. Furthermore, we injected different colours of fluorescent HSCs and MSCs into the tail vein of irradiated mice to reconstruct bone marrow function. We prepared wound models on the back of these mice. In vivo imaging and immunohistochemical staining were used to track the expression of fluorescent protein. Results HSCs and MSCs have been isolated and cultured. HSCs expressed expressed Sca1, not lineage, CD34 or CD48. MSCs expressed expressed CD29 and CD44,not CD34 or CD45. HSCs labeled with green fluorescent protein reached the wound and co-expressed with desmin and α-SMA. MSCs didn’t stay on the wound. Conclusions The results show HSCs in the bone marrow of mice can directly participate in wound healing and differentiate into pericytes and myofibroblasts.


2019 ◽  
Vol 235 (3) ◽  
pp. 2366-2376 ◽  
Author(s):  
Fariba Zafari ◽  
Sadegh Shirian ◽  
Morteza Sadeghi ◽  
Shahram Teimourian ◽  
Mehrdad Bakhtiyari

2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Jinglian Yan ◽  
Guodong Tie ◽  
Shouying Wang ◽  
Amanda Tutto ◽  
Natale DeMarco ◽  
...  

2007 ◽  
Vol 205 (3) ◽  
pp. S66
Author(s):  
Giorgio Pietramaggiori ◽  
Paolo Fiorina ◽  
Saja Scherer ◽  
Jasimine Mathews ◽  
Mollie Jurewicz ◽  
...  

2007 ◽  
Vol 120 (2) ◽  
pp. 407-411 ◽  
Author(s):  
Rodney K. Chan ◽  
Evan Garfein ◽  
Paul R. Gigante ◽  
Perry Liu ◽  
Riaz A. Agha ◽  
...  

2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.


2006 ◽  
Author(s):  
Hideyo Hirai ◽  
Pu Zhang ◽  
Tajhal Dayaram ◽  
Christopher Hetherington ◽  
Shin-ichi Mizuno ◽  
...  

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