Wyniki wyszukiwania - Biblioteka Nauki

1

Heme oxygenase-1 expression in disease states.

100%

Deshane J. , Wright M. , Agarwal A.

Acta Biochimica Polonica

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2005

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tom 52

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nr 2

273-284

EN

Heme oxygenase-1 (HO-1) is an enzyme which catalyzes the rate-limiting step in heme degradation resulting in the formation of iron, carbon monoxide and biliverdin, which is subsequently converted to bilirubin by biliverdin reductase. The biological effects exerted by the products of this enzymatic reaction have gained much attention. The anti-oxidant, anti-inflammatory and cytoprotective functions associated with HO-1 are attributable to one or more of its degradation products. Induction of HO-1 occurs as an adaptive and beneficial response to several injurious stimuli including heme and this inducible nature of HO-1 signifies its importance in several pathophysiological disease states. The beneficial role of HO-1 has been implicated in several clinically relevant disease states involving multiple organ systems as well as significant biological processes such as ischemia-reperfusion injury, inflammation/immune dysfunction and transplantation. HO-1 has thus emerged as a key target molecule with therapeutic implications.

2

Adult stem cells: hopes and hypes of regenerative medicine

100%

Dulak J. , Szade K. , Szade A. , Nowak W. , Józkowicz A.

Acta Biochimica Polonica

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2015

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tom 62

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nr 3

329-337

EN

Stem cells are self-renewing cells that can differentiate into specialized cell type(s). Pluripotent stem cells, i.e. embryonic stem cells (ESC) or induced pluripotent stem cells (iPSC) differentiate into cells of all three embryonic lineages. Multipotent stem cells, like hematopoietic stem cells (HSC), can develop into multiple specialized cells in a specific tissue. Unipotent cells differentiate only into one cell type, like e.g. satellite cells of skeletal muscle. There are many examples of successful clinical applications of stem cells. Over million patients worldwide have benefited from bone marrow transplantations performed for treatment of leukemias, anemias or immunodeficiencies. Skin stem cells are used to heal severe burns, while limbal stem cells can regenerate the damaged cornea. Pluripotent stem cells, especially the patient-specific iPSC, have a tremendous therapeutic potential, but their clinical application will require overcoming numerous drawbacks. Therefore, the use of adult stem cells, which are multipotent or unipotent, can be at present a more achievable strategy. Noteworthy, some studies ascribed particular adult stem cells as pluripotent. However, despite efforts, the postulated pluripotency of such events like "spore-like cells", "very small embryonic-like stem cells" or "multipotent adult progenitor cells" have not been confirmed in stringent independent studies. Also plasticity of the bone marrow-derived cells which were suggested to differentiate e.g. into cardiomyocytes, has not been positively verified, and their therapeutic effect, if observed, results rather from the paracrine activity. Here we discuss the examples of recent studies on adult stem cells in the light of current understanding of stem cell biology.

3

Pharmacological versus genetic inhibition of heme oxygenase-1 - the comparison of metalloporphyrins, shRNA and CRISPR/Cas9 system

86%

Mucha O. , Podkalicka P. , Czarnek M. , Biela A. , Mieczkowski M. , Kachamakova-Trojanowska N. , Stepniewski J. , Jozkowicz A. , Dulak J. , Loboda A.

Acta Biochimica Polonica

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2018

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tom 65

|

nr 2

277-286

EN

Inhibition of heme oxygenase-1 (HO-1, encoded by HMOX1), a cytoprotective, anti-apoptotic and anti-inflammatory enzyme, may serve as a valuable therapy in various pathophysiological processes, including tumorigenesis. We compared the effect of chemical inhibitors - metalloporphyrins, with genetic tools - shRNA and CRISPR/Cas9 systems, to knock-down (KD)/knock-out (KO) HO-1 expression/activity. 293T cells were incubated with metalloporphyrins, tin and zinc protoporphyrins (SnPPIX and ZnPPIX, respectively) or were either transduced with lentiviral vectors encoding different shRNA sequences against HO-1 or were modified by CRISPR/Cas9 system targeting HMOX1. Metalloporphyrins decreased HO activity but concomitantly strongly induced HO-1 mRNA and protein in 293T cells. On the other hand, only slight basal HO-1 inhibition in shRNA KD 293T cell lines was confirmed on mRNA and protein level with no significant effect on enzyme activity. Nevertheless, silencing effect was much stronger when CRISPR/Cas9-mediated knock-out was performed. Most of the clones harboring mutations within HMOX1 locus did not express HO-1 protein and failed to increase bilirubin concentration after hemin stimulation. Furthermore, CRISPR/Cas9-mediated HO-1 depletion decreased 293T viability, growth, clonogenic potential and increased sensitivity to H2O2 treatment. In summary, we have shown that not all technologies can be used for inhibition of HO activity in vitro with the same efficiency. In our hands, the most potent and comprehensible results can be obtained using genetic tools, especially CRISPR/Cas9 approach.

4

Heme oxygenase-1 expression in disease states

86%

Deshane J. , Wright M. , Agarwal A.

Acta Biochimica Polonica

|

2005

|

tom 52

|

nr 2

EN

Heme oxygenase-1 (HO-1) is an enzyme which catalyzes the rate-limiting step in heme degradation resulting in the formation of iron, carbon monoxide and biliverdin, which is subsequently converted to bilirubin by biliverdin reductase. The biological effects exerted by the products of this enzymatic reaction have gained much attention. The anti-oxidant, anti-inflammatory and cytoprotective functions associated with HO-1 are attributable to one or more of its degradation products. Induction of HO-1 occurs as an adaptive and beneficial response to several injurious stimuli including heme and this inducible nature of HO-1 signifies its importance in several pathophysiological disease states. The beneficial role of HO-1 has been implicated in several clinically relevant disease states involving multiple organ systems as well as significant biological processes such as ischemia-reperfusion injury, inflammation/immune dysfunction and transplantation. HO-1 has thus emerged as a key target molecule with therapeutic implications.

5

The effect of hydrogen sulfide-releasing naproxen (ATB-346) versus naproxen on formation of stress-induced gastric lesions. The regulation of systemic inflammation, hypoxia and alterations in gastric microcirculation

72%

Magierowski M. , Magierowska K. , Surmiak M. , Hubalewska-Mazgaj M. , Kwiecien S. , Wallace J. L. , Brzozowski T.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 5

6

Possible role of garlic oil in ameliorating renal injury after liver ischemia/reperfusion in rats

72%

Lasheen N. N. , Elayat W. M. , Elrefai M. F. M. , Zaki W. S. , Ahmed E. H. , El Sheikh R. M. N. , Abo Raya D. S. A. , Gad F. R. S.

Journal of Physiology and Pharmacology

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2019

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tom 70

|

nr 5

7

Genistein exerts a cell-protective effect via Nrf2/HO-1/ /PI3K signaling in A-beta 25-35-induced Alzheimer’s disease models in vitro

72%

Yi S. , Chen S. , Xiang J. , Tan J. , Huang K. , Zhang H. , Wang Y. , Wu H.

Folia Histochemica et Cytobiologica

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2021

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tom 59

|

nr 1

8

Induction of heme oxygenase-1 and heat shock protein 70 in rat hepatocytes: the role of calcium signalling

72%

Silomon M. , Bauer I. , Bauer M. , Nolting J. , Paxian M. , Rensing H.

Cellular and Molecular Biology Letters

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2007

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tom 12

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nr 1

EN

Stress response genes including heat shock proteins are induced under a variety of conditions to confer cellular protection. This study investigated the role of calcium signaling in the induction of two stress response genes, heme oxygenase-1/hsp32 and hsp70, in isolated rat hepatocytes. Both genes were induced by cellular glutathione depletion. This induction could be inhibited by BAPTA-AM. Culturing in a calcium-free medium prevented the induction of hsp70 gene expression after glutathione depletion without affecting heme oxygenase-1 gene expression. Thapsigargin increased the gene expression of heme oxygenase-1 but not that of hsp70. Thapsigargin-induced heme oxygenase-1 induction was completely inhibited by BAPTA-AM. Incubation with the Ca2+-ionophore A23187 augmented heme oxygenase-1 (two-fold) and hsp70 (5.2-fold) mRNA levels. Our data suggests a significant role of Ca2+-dependent pathways in the induction of the two stress genes. An increase in the cytoplasmic Ca2+ activity seems to play a key role in the cascade of signaling leading to the induction of the two genes. However, the source of Ca2+ that fluxes into the cytoplasm seems to be different. Our data provides evidence for a compartmentalization of calcium fluxes, i.e. the Ca2+ flux from intracellular stores (e.g. the endoplasmic reticulum) plays a major role in the induction of heme oxygenase-1. By contrast, Ca2+ flux from the extracellular medium seems to be a mechanism initiating the cellular signaling cascade leading to hsp70 gene induction.

9

Host nuclear factor erythroid 2-related factor 2 defense system determines the outcome of dextran sulfate sodium - induced colitis in mice

58%

Lee J. S. , An J. M. , Kang E. A. , Han Y. M. , Kim Y. S. , Lee H. J. , Kim K.-J. , Surh Y. J. , Hahm K.-B.

Journal of Physiology and Pharmacology

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2018

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tom 69

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nr 5

10

Inhibition of Bach1 ameliorates indomethacin-induced intestinal injury in mice

58%

Harusato A. , Naito Y. , Takagi T. , Yamada S. , Mizushima K. , Hirai Y. , Horie R. , Inoue K. , Fukumoto K. , Hirata I. , Omatsu T. , Kishimoto E. , Uchiyama K. , Handa O. , Ishikawa T. , Kokura S. , Ichikawa H. , Muto A. , Igarashi K. , Yoshikawa T.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

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nr 7

11

Prevention by lansoprazole, a proton pump inhibitor, of indomethacin-induced small intestinal ulceration in rats through induction of heme oxygenase-1

58%

Yoda Y. , Amagase K. , Kato S. , Tokioka S. , Murano M. , Kakimoto K. , Nishio H. , Umegaki E. , Takeuchi K. , Higuchi K.

Journal of Physiology and Pharmacology

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2010

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tom 61

|

nr 3

287-294

EN

The effect of lansoprazole, a proton pump inhibitor (PPI), on indomethacin-induced small intestinal ulceration was examined in rats, particularly in relation to heme oxygenase (HO)-1. The animals were administered indomethacin (10 mg/kg, p.o.) and killed 24 h later. Lansoprazole (30-100 mg/kg, p.o.) and omeprazole (30-100 mg/kg, p.o.) were given 30 min before the administration of indomethacin, while tin-protoporphyrin IX (SnPP: 30 mg/kg, i.v.), an inhibitor of HO-1, was injected 10 min before indomethacin or lansoprazole. Indomethacin produced hemorrhagic lesions in the small intestine, accompanied with an increase of mucosal invasion of enterobacteria, inducible nitric oxide synthase (iNOS) expression, and myeloperoxidase (MPO) activity in the mucosa. Pretreatment with lansoprazole dose- dependently reduced the severity of the indomethacin-induced intestinal lesions, with suppression of the increased MPO activity, while omeprazole had no effect. Pretreatment with SnPP significantly exacerbated these intestinal lesions and almost totally abolished the protective effect of lansoprazole. The up-regulation of iNOS mRNA expression following indomethacin was suppressed by lansoprazole in a SnPP-inhibitable manner, although the enhanced enterobacterial invasion remained unaffected. The amount of HO-1 protein in the intestinal mucosa was significantly increased by lansoprazole but not by omeprazole. Prior administration of carbon monoxide (CO)-releasing molecule-2 (CORM-2; 10 mg/kg, i.p.) significantly reduced the severity of these lesions and the enhancement of mucosal iNOS mRNA expression induced in the small intestine by indomethacin. These results suggest that lansoprazole prevents indomethacin-induced small intestinal ulceration, and this effect is associated with inhibition of iNOS expression, through up-regulation of HO-1/CO production in the mucosa.

12

Metallothioneins in the lung cancer

58%

Werynska B. , Pula B. , Kobierzycki C. , Dziegiel P. , Podhorska-Okolow M.

Folia Histochemica et Cytobiologica

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2015

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tom 53

|

nr 1

13

Molecular alterations in fibroblasts exposed to Helicobacter pylori: a missing link in bacterial inflammation progressing into gastric carcinogenesis?

58%

Krzysiek-Maczka G. , Targosz A. , Ptak-Belowska A. , Korbut E. , Szczyrk U. , Strzalka M. , Brzozowski T.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 1

14

Aging and expression of heme oxygenase-1 and endothelin-1 in the rat carotid body after chronic hypoxia

58%

Di Giulio C. , Verratti V. , Artese L. , Petruccelli G. , Walski M. , Pokorski M.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

|

nr 5

15

Myokine irisin-induced protection against oxidative stress in vitro. Involvement of heme oxygenase-1 and antioxidazing enzymes superoxide dismutase-2 and glutathione peroxidase

58%

Mazur-Bialy A. I. , Kozlowska K. , Pochec E. , Bilski J. , Brzozowski T.

Journal of Physiology and Pharmacology

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2018

|

tom 69

|

nr 1

16

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

58%

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

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2009

|

tom 60

|

nr 2

3-12

EN

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.

17

Dietary threonine prevented stress-related mucosal diseases in rats

58%

An J. M. , Kang E. A. , Han Y. M. , Kim Y. S. , Hong Y. G. , Hah B. S. , Hong S. P. , Hahm K. B.

Journal of Physiology and Pharmacology

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2019

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tom 70

|

nr 3

18

Therapeutic potential of heme oxygenase-1 in cardiovascular disease

51%

Jazwa A. , Florczyk U. , Stepniewski J. , Jozkowicz A. , Dulak J.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2011

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tom 92

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nr 2