Axonal degeneration in an in vitro model of ischemic white matter injury

1. We used an in vitro model to explore critical aspects of chronic epileptogenesis. Partial neocortical isolations having intact blood supply were made in rat and guinea pig from postnatal day 7 to 34 and then examined 1 to 150 days later in standard brain slice preparations. 2. The epileptogenic potential of several different types of lesions was assessed. Slices containing transcortical (i.e., gray matter) lesions, with or without a contiguous white matter injury (i.e., “undercut”), developed chronic epileptogenesis after a latency of approximately 1–2 wk, manifested by evoked and spontaneous “interictal” discharges and evoked “ictal” events. The region of hyperexcitability did not extend beyond approximately 2 mm from the chronic transcortical lesion and was rarely observed in slices having only an apparent white matter injury. 3. Multiple recordings and current source density (CSD) analysis identified layer V as the source of the interictal discharge. 4. Significant differences in CSD profiles of the evoked interictal discharge occurred between chronically epileptogenic slices and control (noninjured) slices bathed in the convulsant, bicuculline methiodide, suggesting that mechanisms other than disinhibition must be involved in posttraumatic epileptogenesis. 5. Interictal events were blocked in most but not all chronically injured slices by application of the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovalerate (D-AP5), suggesting that non-NMDA receptors were predominantly involved in some preparations. 6. This model of chronic epileptogenesis in vitro will be useful in studies relevant to mechanisms of posttraumatic epilepsy in man.

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Astrocyte-forebrain co-cultures: an in vitro model for studying the role of astrocytes in childhood white matter disorders

Tijdschrift voor kindergeneeskunde ◽

10.1007/s12456-013-0065-3 ◽

2013 ◽

Vol 81 (S1) ◽

pp. 66-66

Author(s):

Melanie D. Klok ◽

Stephanie Dooves ◽

Carola G.M. van Berkel ◽

Wia Baron ◽

Christine E. Thomson ◽

...

Keyword(s):

White Matter ◽

In Vitro Model ◽

White Matter Disorders ◽

Vitro Model

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An in vitro model for investigation of vitamin A effects on wound healing

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000692 ◽

2021 ◽

pp. 1-6

Author(s):

Hoda Keshmiri Neghab ◽

Mohammad Hasan Soheilifar ◽

Gholamreza Esmaeeli Djavid

Keyword(s):

Wound Healing ◽

Endothelial Cell ◽

Vitamin A ◽

In Vitro Model ◽

Cellular Proliferation ◽

Endothelial Cell Migration ◽

Normal Fibroblast ◽

Anti Inflammatory ◽

Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inﬂammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inﬂammation responses.

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