Role of glutamate and its receptors and insulin-like growth factors in hypoxia induced periventricular white matter injury

Glia ◽  
2009 ◽  
Vol 58 (5) ◽  
pp. 507-523 ◽  
Author(s):  
Viswanathan Sivakumar ◽  
Eng-Ang Ling ◽  
Jia Lu ◽  
Charanjit Kaur
Keyword(s):  
Growth Factors ◽  
White Matter ◽  
White Matter Injury ◽  
Periventricular White Matter ◽  
Insulin Like Growth Factors

scholarly journals Important Role of Reverse Na+-Ca2+Exchange in Spinal Cord White Matter Injury at Physiological Temperature

2000 ◽  
Vol 84 (2) ◽  
pp. 1116-1119 ◽  
Author(s):  
Shuxin Li ◽  
Qiubo Jiang ◽  
Peter K. Stys
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Traumatic Injury ◽  
White Matter Injury ◽  
Mechanical Trauma ◽  
White Matter Tracts ◽  
Physiological Temperature ◽  
Cord Injury ◽  
Cellular Ca

Spinal cord injury is a devastating condition in which most of the clinical disability results from dysfunction of white matter tracts. Excessive cellular Ca2+ accumulation is a common phenomenon after anoxia/ischemia or mechanical trauma to white matter, leading to irreversible injury because of overactivation of multiple Ca2+-dependent biochemical pathways. In the present study, we examined the role of Na+-Ca2+ exchange, a ubiquitous Ca2+ transport mechanism, in anoxic and traumatic injury to rat spinal dorsal columns in vitro. Excised tissue was maintained in a recording chamber at 37°C and injured by exposure to an anoxic atmosphere for 60 min or locally compressed with a force of 2 g for 15 s. Mean compound action potential amplitude recovered to ≈25% of control after anoxia and to ≈30% after trauma. Inhibitors of Na+-Ca2+ exchange (50 μM bepridil or 10 μM KB-R7943) improved functional recovery to ≈60% after anoxia and ≈70% after traumatic compression. These inhibitors also prevented the increase in calpain-mediated spectrin breakdown products induced by anoxia. We conclude that, at physiological temperature, reverse Na+-Ca2+exchange plays an important role in cellular Ca2+ overload and irreversible damage after anoxic and traumatic injury to dorsal column white matter tracts.

The Potential Role of Insulin-Like Growth Factors in Skeletal Muscle Regeneration

1996 ◽  
Vol 21 (4) ◽  
pp. 236-250 ◽  
Author(s):  
Jamie MacGregor ◽  
Wade S. Parkhouse
Keyword(s):  
Skeletal Muscle ◽  
Growth Hormone ◽  
Growth Factors ◽  
Muscle Regeneration ◽  
Potential Role ◽  
Tissue Growth ◽  
Skeletal Muscle Regeneration ◽  
Tissue Type ◽  
Insulin Like Growth Factors

The role of the insulin-like growth factors I and II (IGF-I and IGF-II), previously known as the somatomedins, in general growth and development of various tissues has been known for many years. Thought of exclusively as endocrine factors produced by the liver, and under the control of growth hormone, the somatomedins were known as the intermediaries by which growth hormone exerted its cellular effects during tissue growth and maturation. Eventually it was discovered that virtually every tissue type is capable of autocrine production of the IGFs, and their involvement in skeletal muscle tissue repair and regeneration became apparent. Recent advances in technology have allowed the characterisation of many of the different growth factors believed to play a role in muscle regeneration, and experimental manipulations of cells in culture have provided insight into the effects of the various growth factors on the myoblast. This paper explores the potential role of the IGFs in skeletal muscle regeneration. A critical role of IGF-II in terminal differentiation of proliferating muscle precurser cells following injury is proposed. Key words: growth factors, myogenesis, skeletal muscle regeneration

scholarly journals A Systematic Review of WNT Signaling in Endothelial Cell Oligodendrocyte Interactions: Potential Relevance to Cerebral Small Vessel Disease

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1545
Author(s):  
Narek Manukjan ◽  
Zubair Ahmed ◽  
Daniel Fulton ◽  
W. Matthijs Blankesteijn ◽  
Sébastien Foulquier
Keyword(s):  
White Matter ◽  
Small Vessel Disease ◽  
Clinical Manifestations ◽  
Cell Types ◽  
Cerebral Small Vessel Disease ◽  
White Matter Injury ◽  
Small Vessel ◽  
Limited Attention ◽  
Vessel Disease

Key pathological features of cerebral small vessel disease (cSVD) include impairment of the blood brain barrier (BBB) and the progression of white matter lesions (WMLs) amongst other structural lesions, leading to the clinical manifestations of cSVD. The function of endothelial cells (ECs) is of major importance to maintain a proper BBB. ECs interact with several cell types to provide structural and functional support to the brain. Oligodendrocytes (OLs) myelinate axons in the central nervous system and are crucial in sustaining the integrity of white matter. The interplay between ECs and OLs and their precursor cells (OPCs) has received limited attention yet seems of relevance for the study of BBB dysfunction and white matter injury in cSVD. Emerging evidence shows a crosstalk between ECs and OPCs/OLs, mediated by signaling through the Wingless and Int-1 (WNT)/β-catenin pathway. As the latter is involved in EC function (e.g., angiogenesis) and oligodendrogenesis, we reviewed the role of WNT/β-catenin signaling for both cell types and performed a systematic search to identify studies describing a WNT-mediated interplay between ECs and OPCs/OLs. Dysregulation of this interaction may limit remyelination of WMLs and render the BBB leaky, thereby initiating a vicious neuroinflammatory cycle. A better understanding of the role of this signaling pathway in EC–OL crosstalk is essential in understanding cSVD development.

Sign in / Sign up

Export Citation Format

Share Document