Delayed cutaneous wound closure in HO ‐2 deficient mice despite normal HO ‐1 expression
نویسندگان
چکیده
منابع مشابه
Delayed cutaneous wound closure in HO-2 deficient mice despite normal HO-1 expression
Impaired wound healing can lead to scarring, and aesthetical and functional problems. The cytoprotective haem oxygenase (HO) enzymes degrade haem into iron, biliverdin and carbon monoxide. HO-1 deficient mice suffer from chronic inflammatory stress and delayed cutaneous wound healing, while corneal wound healing in HO-2 deficient mice is impaired with exorbitant inflammation and absence of HO-1...
متن کاملHeme Oxygenase-1 Accelerates Cutaneous Wound Healing in Mice
Heme oxygenase-1 (HO-1), a cytoprotective, pro-angiogenic and anti-inflammatory enzyme, is strongly induced in injured tissues. Our aim was to clarify its role in cutaneous wound healing. In wild type mice, maximal expression of HO-1 in the skin was observed on the 2(nd) and 3(rd) days after wounding. Inhibition of HO-1 by tin protoporphyrin-IX resulted in retardation of wound closure. Healing ...
متن کاملThe Role of Neutrophils in Corneal Wound Healing in HO-2 Null Mice
Our studies demonstrated that Heme oxygenase (HO), in particular, the constitutive HO-2, is critical for a self-resolving inflammatory and repair response in the cornea. Epithelial injury in HO-2 null mice leads to impaired wound closure and chronic inflammation in the cornea. This study was undertaken to examine the possible relationship between HO-2 and the recruitment of neutrophils followin...
متن کاملKinetics of HO 2 + HO 2 ! H 2 O 2 + O 2 : Implications for Stratospheric H
[1] The reaction HO2 + HO2 ! H2O2 + O2 (1) has been studied at 100 Torr and 222 K to 295 K. Experiments employing photolysis of Cl2/CH3OH/O2/N2 and F2/H2/O2/N2 gas mixtures to produce HO2 confirmed that methanol enhanced the observed reaction rate. At 100 Torr, zero methanol, k1 = (8.8 ± 0.9) 10 13 exp[(210 ± 26)/T] cm molecule 1 s 1 (2s uncertainties), which agrees with current recommendations...
متن کاملCO/HO-1 Induces NQO-1 Expression via Nrf2 Activation
BACKGROUND Carbon monoxide (CO) is a cytoprotective and homeostatic molecule with important signaling capabilities in physiological and pathophysiological situations. CO protects cells/tissues from damage by free radicals or oxidative stress. NAD(P)H:quinone oxidoreductase (NQO1) is a highly inducible enzyme that is regulated by the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor ery...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Cellular and Molecular Medicine
سال: 2014
ISSN: 1582-1838,1582-4934
DOI: 10.1111/jcmm.12389