scholarly journals The bone morphogenetic protein antagonist noggin protects white matter after perinatal hypoxia–ischemia

2011 ◽  
Vol 42 (3) ◽  
pp. 318-326 ◽  
Author(s):  
Maria L.V. Dizon ◽  
Tensing Maa ◽  
John A. Kessler
Keyword(s):  
White Matter ◽  
Bone Morphogenetic Protein ◽  
Perinatal Hypoxia ◽  
Morphogenetic Protein ◽  
Hypoxia Ischemia

Alteration in rectification of potassium channels in perinatal hypoxia ischemia brain damage

2015 ◽  
Vol 113 (2) ◽  
pp. 592-600 ◽  
Author(s):  
Penghui Chen ◽  
Liyan Wang ◽  
Qiyue Deng ◽  
Huaizhen Ruan ◽  
Wenqin Cai
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Brain Damage ◽  
Lucifer Yellow ◽  
Membrane Resistance ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
High Signal ◽  
Perinatal Hypoxia ◽  
Hypoxia Ischemia

Oligodendrocyte progenitor cells (OPCs) are susceptible to perinatal hypoxia ischemia brain damage (HIBD), which results in infant cerebral palsy due to the effects on myelination. The origin of OPC vulnerability in HIBD, however, remains controversial. In this study, we defined the HIBD punctate lesions by MRI diffuse excessive high signal intensity (DEHSI) in postnatal 7-day-old rats. The electrophysiological functional properties of OPCs in HIBD were recorded by patch-clamp in acute cerebral cortex slices. The slices were intracellularly injected with Lucifer yellow and immunohistochemically labeled with NG2 antibody to identify local OPCs. Passive membrane properties and K+ channel functions in OPCs were analyzed to estimate the onset of vulnerability in HIBD. The resting membrane potential, membrane resistance, and membrane capacitance of OPCs were increased in both the gray and white matter of the cerebral cortex. OPCs in both the gray and white matter exhibited voltage-dependent K+ currents, which consisted of the initiated rectified potassium currents ( IA) and the sustained rectified currents ( IK). The significant alternation in membrane resistance was influenced by the diversity of potassium channel kinetics. These findings suggest that the rectification of IA and IK channels may play a significant role in OPC vulnerability in HIBD.

Perinatal Hypoxia-Ischemia Induces Apoptotic and Excitotoxic Death of Periventricular White Matter Oligodendrocyte Progenitors

2001 ◽  
Vol 23 (3) ◽  
pp. 203-208 ◽  
Author(s):  
Jennifer K. Ness ◽  
Michael J. Romanko ◽  
Raymond P. Rothstein ◽  
Teresa L. Wood ◽  
Steven W. Levison
Keyword(s):  
White Matter ◽  
Periventricular White Matter ◽  
Perinatal Hypoxia ◽  
Oligodendrocyte Progenitors ◽  
Hypoxia Ischemia

scholarly journals Pericyte-derived bone morphogenetic protein 4 underlies white matter damage after chronic hypoperfusion

2017 ◽  
Vol 28 (4) ◽  
pp. 521-535 ◽  
Author(s):  
Maiko T. Uemura ◽  
Masafumi Ihara ◽  
Takakuni Maki ◽  
Takayuki Nakagomi ◽  
Seiji Kaji ◽  
...  
Keyword(s):  
White Matter ◽  
Bone Morphogenetic Protein ◽  
Bone Morphogenetic Protein 4 ◽  
White Matter Damage ◽  
Morphogenetic Protein

Oxygen treatment after perinatal hypoxia-ischemia reduces neuronal damage at short survival times, but worsens injury with long-term survival

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S444-S444 ◽  
Author(s):  
Kristin M Noppens ◽  
J Regino Perez-Polo ◽  
David K Rassin ◽  
Karin N Westlund ◽  
Roderic Fabian ◽  
...  
Keyword(s):  
Neuronal Damage ◽  
Perinatal Hypoxia ◽  
Survival Times ◽  
Term Survival ◽  
Long Term Survival ◽  
Short Survival ◽  
Oxygen Treatment ◽  
Hypoxia Ischemia

Expression, signalling and potential in vivo functions of Bone Morphogenetic Protein (BMP)-9 in the liver

2009 ◽  
Vol 47 (01) ◽  
Author(s):  
K Breitkopf ◽  
A Müller ◽  
L Ciuclan ◽  
E Wiercinska ◽  
P ten Dijke ◽  
...  
Keyword(s):  
Bone Morphogenetic Protein ◽  
Morphogenetic Protein
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