Motor behavioral abnormalities and histopathological findings of Wistar rats inoculated with HTLV-1-infected MT2 cells

Câmara, Carlos Campos; Oriá, Reinaldo B.; Felismino, T.C.; Silva, A.P. da; Silva, M.A.M. da; Alcantara, Jorge; Costa, S.B.C.; Vicente, Ana Carolina Paulo; Teixeira-Santos, T.J.; Castro-Costa, Carlos Maurício de

doi:10.1590/s0100-879x2010007500050

Cited by 4 publications

(2 citation statements)

References 19 publications

(19 reference statements)

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“…As the 15-20 month-old rats correspond to 60-year-old humans (Câ mara, et al, 2010;Culter, et al, 2007), 20-month-old rats were used in this study.…”

mentioning

confidence: 99%

Progesterone Increases Circulating Endothelial Progenitor Cells and Induces Neural Regeneration after Traumatic Brain Injury in Aged Rats

Wang

Kan

et al. 2012

Journal of Neurotrauma

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Vascular remodeling plays a key role in neural regeneration in the injured brain. Circulating endothelial progenitor cells (EPCs) are a mediator of the vascular remodeling process. Previous studies have found that progesterone treatment of traumatic brain injury (TBI) decreases cerebral edema and cellular apoptosis and inhibits inflammation, which in concert promote neuroprotective effects in young adult rats. However, whether progesterone treatment regulates circulating EPC level and fosters vascular remodeling after TBI have not been investigated. In this study, we hypothesize that progesterone treatment following TBI increases circulating EPC levels and promotes vascular remodeling in the injured brain in aged rats. Male Wistar 20-month-old rats were subjected to a moderate unilateral parietal cortical contusion injury and were treated with or without progesterone (n = 54/group). Progesterone was administered intraperitoneally at a dose of 16mg/kg at 1 h post-TBI and was subsequently injected subcutaneously daily for 14 days. Neurological functional tests and immnunostaining were performed. Circulating EPCs were measured by flow cytometry. Progesterone treatment significantly improved neurological outcome after TBI measured by the modified neurological severity score, Morris Water Maze and the long term potentiation in the hippocampus as well as increased the circulating EPC levels compared to TBI controls ( p < 0.05). Progesterone treatment also significantly increased CD34 and CD31 positive cell number and vessel density in the injured brain compared to TBI controls ( p < 0.05). These data indicate that progesterone treatment of TBI improves multiple neurological functional outcomes, increases the circulating EPC level, and facilitates vascular remodeling in the injured brain after TBI in aged rats.

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“…As the 15-20 month-old rats correspond to 60-year-old humans (Câ mara, et al, 2010;Culter, et al, 2007), 20-month-old rats were used in this study.…”

mentioning

confidence: 99%

Progesterone Increases Circulating Endothelial Progenitor Cells and Induces Neural Regeneration after Traumatic Brain Injury in Aged Rats

Wang

Kan

et al. 2012

Journal of Neurotrauma

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“…71 However, a recent report found that HTLV-1-infected Wistar rats showed diffuse lymphocyte infiltration in some cases. 73 Other studies using HTLV-1infected rats reported selective activation of HTLV-1 pX and tumor necrosis factor (TNF)-α mRNA in target spinal cord and peripheral nerves, altered expression of bcl-2, bax, and p53 apoptosis-regulating genes in lesions, and interferon (IFN)-γ production in spinal cord lesions. 69,70,74,75 HTLV-1 proviral DNA has also been found in lesion-associated microglial cells and macrophages of infected animals.…”

Section: Rabbit Modelmentioning

confidence: 99%

Animal Models Utilized in HTLV-1 Research

2013

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Since the isolation and discovery of human T-cell leukemia virus type 1 (HTLV-1) over 30 years ago, researchers have utilized animal models to study HTLV-1 transmission, viral persistence, virus-elicited immune responses, and HTLV-1-associated disease development (ATL, HAM/TSP). Non-human primates, rabbits, rats, and mice have all been used to help understand HTLV-1 biology and disease progression. Non-human primates offer a model system that is phylogenetically similar to humans for examining viral persistence. Viral transmission, persistence, and immune responses have been widely studied using New Zealand White rabbits. The advent of molecular clones of HTLV-1 has offered the opportunity to assess the importance of various viral genes in rabbits, non-human primates, and mice. Additionally, over-expression of viral genes using transgenic mice has helped uncover the importance of Tax and Hbz in the induction of lymphoma and other lymphocyte-mediated diseases. HTLV-1 inoculation of certain strains of rats results in histopathological features and clinical symptoms similar to that of humans with HAM/TSP. Transplantation of certain types of ATL cell lines in immunocompromised mice results in lymphoma. Recently, “humanized” mice have been used to model ATL development for the first time. Not all HTLV-1 animal models develop disease and those that do vary in consistency depending on the type of monkey, strain of rat, or even type of ATL cell line used. However, the progress made using animal models cannot be understated as it has led to insights into the mechanisms regulating viral replication, viral persistence, disease development, and, most importantly, model systems to test disease treatments.

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HTLV-1 infection-induced motor dysfunction, memory impairment, depression, and brain tissues oxidative damage in female BALB/c mice

et al. 2018

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Motor behavioral abnormalities and histopathological findings of Wistar rats inoculated with HTLV-1-infected MT2 cells

Cited by 4 publications

References 19 publications

Progesterone Increases Circulating Endothelial Progenitor Cells and Induces Neural Regeneration after Traumatic Brain Injury in Aged Rats

Progesterone Increases Circulating Endothelial Progenitor Cells and Induces Neural Regeneration after Traumatic Brain Injury in Aged Rats

Animal Models Utilized in HTLV-1 Research

HTLV-1 infection-induced motor dysfunction, memory impairment, depression, and brain tissues oxidative damage in female BALB/c mice

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