CD161a-positive natural killer (NK) cells and α-smooth muscle actin-positive myofibroblasts were upregulated by extrarenal DPP4 in a rat model of acute renal rejection

2021 ◽  
Vol 173 ◽  
pp. 108691
Author(s):  
Franziska Schmid ◽  
Christina Mayer ◽  
Maike Büttner-Herold ◽  
Stephan von Hörsten ◽  
Kerstin Amann ◽  
...  
2012 ◽  
Vol 32 (11) ◽  
pp. 2055-2065 ◽  
Author(s):  
Varun Sharma ◽  
Tina W Ling ◽  
Sarah S Rewell ◽  
David L Hare ◽  
David W Howells ◽  
...  

In a rat model of stroke, the spatio-temporal distribution of α-smooth muscle actin-positive, (αSMA+) cells was investigated in the infarcted hemisphere (ipsilateral) and compared with the contralateral hemisphere. At day 3 postischemia, αSMA+ cells were concentrated in two main loci within the ipsilateral hemisphere (Area A) in the medial corpus callosum and (Area B) midway through the striatum adjacent to the lateral ventricle. By day 7 and further by day 14, fewer αSMA+ cells remained in Areas A and B but a steady increase in the peri-infarct was observed. αSMA+ cells also expressed glial acidic fibrillary protein [GFAP: αSMA+/GFAP+ (29%); αSMA+/GFAP– (71%) phenotypes] and feline leukemia virus C receptor 2 (FLVCR2), but not ED1(microglia) and established markers of pericytes normally located in vascular wall. αSMA+ cells were also located close to the subventricular zones (SVZ) adjacent to Areas A and B. In conclusion, αSMA + cells have been identified in a spatial and temporal sequence from the SVZ, at intermediate loci and in the vicinity of the peri-infarct. It is hypothesized that novel populations of αSMA+ precursors of pericytes are born on the SVZ, migrate into the peri-infarct region and are incorporated into new vessels of the peri-infarct regions.


2008 ◽  
Vol 180 (1) ◽  
pp. 388-391 ◽  
Author(s):  
Marc Olivier Timsit ◽  
Rudy Gadet ◽  
Hassen Ben Abdennebi ◽  
Ricardo Codas ◽  
Palmina Petruzzo ◽  
...  

2003 ◽  
Vol 21 (1) ◽  
pp. 20-27 ◽  
Author(s):  
B. Kinner ◽  
D. M. Pacicca ◽  
L. C. Gerstenfeld ◽  
C. A. Lee ◽  
T. A. Einhorn ◽  
...  

2021 ◽  
Vol 11 (8) ◽  
pp. 3524
Author(s):  
Azeem Ul Yaqin Syed ◽  
Muhammad A. Ahmed ◽  
Eman I. AlSagob ◽  
Mansour Al-Askar ◽  
Abdulrahman M. AlMubarak ◽  
...  

The aim was to determine the cytotoxicity of Khat (Catha edulis (Vahl) Forssk. ex Endl) on normal oral fibroblasts (NOFs) and SCC4 (squamous carcinoma cells) along with expression of α-smooth muscle actin (α-SMA) in fibroblasts. Khat filtrate was prepared to obtain a concentrated viscous solution. NOFs and SCC4 cells were cultured in biological cabinets and were grown in Dulbeccos’ modified Eagles medium. Frozen cells were thawed at 37 °C and cell seeding was performed. NOFs and SCC4 cells were seeded on 96 well plates and allowed to attach. The medium was removed and a fresh medium containing different concentrations of Khat was added. The group without Khat served as a negative control and 4% paraformaldehyde as the positive control. Cell viability was assessed using the MTT assay and effect of Khat on fibroblast and SCC4 phenotypes was evaluated by immunostaining. Analysis of variance was used to assess data (p < 0.05). NOF 316 showed cell death in response to 4% paraformaldehyde, 12.5, 6.25, and 3.12 mg/mL of Khat. The highest concentration of Khat (25 mg/mL) failed to cause cytotoxicity of NOF 316. NOF 319 and NOF 26 displayed cell death at all concentrations of Khat, however, cytotoxicity was not dose dependent. NOF 18 and SCC4 cells showed dose-dependent cell death. NOF 316 showed α-SMA expression after 1 mg/mL of Khat exposure. Not all fibroblasts were α-SMA-positive, suggesting specific activation of a subset of fibroblasts. Khat is cytotoxic to NOF and SCC4 cells. Furthermore, it can also cause activation and phenotypic changes in oral fibroblasts, indicating a potential role in progression of oral squamous cell carcinoma.


1997 ◽  
Vol 33 (8) ◽  
pp. 622-627 ◽  
Author(s):  
M. Reza Ghassemifar ◽  
Roy W. Tarnuzzer ◽  
Nasser Chegini ◽  
Erkki Tarpila ◽  
Gregory S. Schultz ◽  
...  

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