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1

PCR - czyli jak pomnozyc niewidzialne

100%
Kotlinowski J.
Wszechświat
|
2005
|
tom 106
|
nr 01-03
71-74
2

Proangiogenna terapia komorkowa: obiecujaca perspektywa czy zludna nadzieja?

45%
Grochot-Przeczek A., Szade K., Kotlinowski J., Jozkowicz A., Dulak J.
Postępy Biologii Komórki
|
2010
|
tom 37
|
nr 1
167-186
3

Rola genow antyoksydacyjnych w komorkach progenitorowych srodblonka i miesniowych komorkach satelitarnych

39%
Kozakowska M., Florczyk U., Grochot-Przeczek A., Kotlinowski J., Jozkowicz A., Dulak J.
Postępy Biologii Komórki
|
2010
|
tom 37
|
nr 1
137-151
4

Cukrzyca a komorki progenitorowe srodblonka

39%
Kotlinowski J., Kozakowska M., Grochot-Przeczek A., Kotlinowska B., Jozkowicz A., Dulak J.
Postępy Biologii Komórki
|
2010
|
tom 37
|
nr 1
153-165
5

HO-1 regulates expression of human MMP-1 and murine MMP-13 in vitro

33%
Golda S., Kabala P., Sokolowska M., Stopa M., Kotlinowski J., Sierpnowska A., Jozkowicz A., Boczkowski J., Dulak J.
Acta Biochimica Polonica
|
2007
|
tom 54
|
nr Supplement 4
6

Effects of heme oxygenase-1 on proliferation, cell cycle regulation and susceptibility of the primary murine fibroblasts to oxidative stress

33%
Kotlinowski J., Kabala P., Lackowska B., Grochot-Przeczek A., Sokolowska M., Dominik P., Sierpniowska A., Dulak J., Jozkowicz A.
Acta Biochimica Polonica
|
2007
|
tom 54
|
nr Supplement 4
7
Content available remote

Transient and stable transfections of mouse myoblasts with genes coding for pro-angiogenic factors

33%
Bialas M., Krupka M., Janeczek A., Rozwadowska N., Fraczek M., Kotlinowski J., Kucharzewska P., Lackowska B., Kurpisz M.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 2
Cardiomyocyte loss in the ischaemic heart can be the reason of many complications, eventually being even the cause of patient's death. Despite many promises, cell therapy with the use of skeletal muscle stem cells (SMSC) still remains to be modified and improved. Combined cell and gene therapy seems to be a promising strategy to heal damaged myocardium. In the present study we have investigated the influence of a simultaneous overexpression of two potent pro-angiogenic genes encoding the fibroblast growth factor-4 (FGF-4) and the vascular endothelial growth factor-A (VEGF-A) on a myogenic murine C2C12 cell line. We have demonstrated in in vitro conditions that myoblasts which overexpressed these factors exhibited significant changes in the cell cycle and pro-angiogenic potential with only slight differences in the expression of the myogenic genes. There was not observed the influence of transient or stable overexpression of FGF-4 and VEGF on cell apoptosis/necrosis in standard or oxidative stress conditions comparing to non transfected controls. Overall, our results suggest that the possible transplantation of myoblasts overexpressing pro-angiogenic factors may potentially improve the functionality of the injured myocardium although the definite proof must originate from in situ conducted pre-clinical studies.
8
Content available remote

Modulation of inflammatory response by pentoxifylline is independent of heme oxygenase-1 pathway

27%
Taha H., Grochot-Przeczek A., Was H., Kotlinowski J., Kozakowska M., Marek A., Skrzypek K., Lackowska B., Balcerczyk A., Mustafa S., Dulak J., Jozkowicz A.
Journal of Physiology and Pharmacology
|
2009
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tom 60
|
nr 2
3-12
Objective: It was reported that some effects of pentoxifylline (PTX) are mediated by heme oxygenase-1 (HO-1) induction. We investigated the role of HO-1 in anti-inflammatory activity of PTX. Methods: Experiments were performed in human and murine monocytes and endothelial cells and in HO-1 deficient mice. Results: PTX dose-dependently decreased expression of HO-1 in cell lines studied. As expected, PTX reduced also production of TNF. This effect was independent of HO-1 activity, as demonstrated in cells treated with HO-1 activators and inhibitors or in cells overexpressing HO-1. Moreover, inhibition of TNF was the same in human endothelial cells of different HO-1 genotypes, showing that PTX is similarly efficient in carriers of more and less active HO-1 promoter variants. In mice, PTX did not influence HO-1 expression, as measured in liver, kidney, spleen, heart, and skin. Accordingly, the response of PTX treated animals to LPS was the same in wild type and HO-1 deficient mice. PTX to a similar extent increased influx of leukocyte into peritoneal cavity, decreased production of TNF and reduced expression of VCAM-1 in vascular intima. Conclusion: PTX inhibits production of TNF and may decrease inflammatory reaction both in vitro and in vivo, but these effects are independent of HO-1.
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