Journal of Pathology and Translational Medicine

Original Articles

An Experimental Infarct Targeting the Internal Capsule: Histopathological and Ultrastructural Changes: Chang-Woo Han, Kyung-Hwa Lee, Myung Giun Noh, Jin-Myung Kim, Hyung-Seok Kim, Hyung-Sun Kim, Ra Gyung Kim, Jongwook Cho, Hyoung-Ihl Kim, Min-Cheol Lee; J Pathol Transl Med. 2017;51(3):292-305. Published online May 10, 2017; DOI: https://doi.org/10.4132/jptm.2017.02.17

8,212 View
113 Download
5 Web of Science
6 Crossref

Background
Stroke involving the cerebral white matter (WM) has increased in prevalence, but most experimental studies have focused on ischemic injury of the gray matter. This study was performed to investigate the WM in a unique rat model of photothrombotic infarct targeting the posterior limb of internal capsule (PLIC), focusing on the identification of the most vulnerable structure in WM by ischemic injury, subsequent glial reaction to the injury, and the fundamental histopathologic feature causing different neurologic outcomes.
Methods
Light microscopy with immunohistochemical stains and electron microscopic examinations of the lesion were performed between 3 hours and 21 days post-ischemic injury.
Results
Initial pathological change develops in myelinated axon, concomitantly with reactive change of astrocytes. The first pathology to present is nodular loosening to separate the myelin sheath with axonal wrinkling. Subsequent pathologies include rupture of the myelin sheath with extrusion of axonal organelles, progressive necrosis, oligodendrocyte degeneration and death, and reactive gliosis. Increase of glial fibrillary acidic protein (GFAP) immunoreactivity is an early event in the ischemic lesion. WM pathologies result in motor dysfunction. Motor function recovery after the infarct was correlated to the extent of PLIC injury proper rather than the infarct volume.
Conclusions
Pathologic changes indicate that the cerebral WM, independent of cortical neurons, is highly vulnerable to the effects of focal ischemia, among which myelin sheath is first damaged. Early increase of GFAP immunoreactivity indicates that astrocyte response initially begins with myelinated axonal injury, and supports the biologic role related to WM injury or plasticity. The reaction of astrocytes in the experimental model might be important for the study of pathogenesis and treatment of the WM stroke.

Citations

Citations to this article as recorded by

Animal models of focal ischemic stroke: brain size matters
Blazej Nowak, Piotr Rogujski, Raphael Guzman, Piotr Walczak, Anna Andrzejewska, Miroslaw Janowski
Frontiers in Stroke.2023;[Epub] CrossRef
Motor Cortex Plasticity During Functional Recovery Following Brain Damage
Noriyuki Higo
Journal of Robotics and Mechatronics.2022; 34(4): 700. CrossRef
Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat
Tatiana Anan’ina, Alena Kisel, Marina Kudabaeva, Galina Chernysheva, Vera Smolyakova, Konstantin Usov, Elena Krutenkova, Mark Plotnikov, Marina Khodanovich
International Journal of Molecular Sciences.2020; 21(17): 6246. CrossRef
Quantitative assessment of demyelination in ischemic stroke in vivo using macromolecular proton fraction mapping
Marina Y Khodanovich, Alena A Kisel, Andrey E Akulov, Dmitriy N Atochin, Marina S Kudabaeva, Valentina Y Glazacheva, Michael V Svetlik, Yana A Medvednikova, Lilia R Mustafina, Vasily L Yarnykh
Journal of Cerebral Blood Flow & Metabolism.2018; 38(5): 919. CrossRef
Immunosignals of Oligodendrocyte Markers and Myelin-Associated Proteins Are Critically Affected after Experimental Stroke in Wild-Type and Alzheimer Modeling Mice of Different Ages
Dominik Michalski, Anna L. Keck, Jens Grosche, Henrik Martens, Wolfgang Härtig
Frontiers in Cellular Neuroscience.2018;[Epub] CrossRef
Administration of Downstream ApoE Attenuates the Adverse Effect of Brain ABCA1 Deficiency on Stroke
Xiaohui Wang, Rongwen Li, Alex Zacharek, Julie Landschoot-Ward, Fengjie Wang, Kuan-Han Hank Wu, Michael Chopp, Jieli Chen, Xu Cui
International Journal of Molecular Sciences.2018; 19(11): 3368. CrossRef

The Effect of Ribbon-Type Antisense Oligodeoxynucleotides for Transforming Growth Factor-beta1 in Unilateral Ureteral Obstruction .: Sang Mi Han, Eun Joo Kim, Hyo Soon Jeoung, Byung Yuk Lee, Sang Sook Lee, Kwan Kyu Park, Hyun Chul Kim; Korean J Pathol. 2002;36(2):84-92.

1,464 View
16 Download

Abstract PDF: BACKGROUND
In unilateral ureteral obstruction (UUO), the obstructed kidney is characterized by interstitial fibrosis and an increase in transforming growth factor (TGF)-beta1. Interstitial expression of TGF-beta1 is important in tublointerstitial fibrosis. The objectives of this study is to make new ribbon-type antisense oligodeoxynucleotides (ODN) for TGF-beta1 which are resistant to exonuclease and to examine the effcets of TGF-beta1 on reducing tubulointerstitial fibrosis of the kidney.
METHODS
We introduced a new ribbon-type antisense ODN for TGF-beta1 in rats using the UUO model to block interstitial fibrosis by tail vein injection. A combination of one antisense sequences for TGF-beta1 was adopted to construct a large antisense molecule with a loop and stem. Artificial viral envelope (AVE)-type hemagglutinating virus of Japan (HVJ)-liposomes were used as a vector system for the delivery of antisense ODN.
RESULTS
The levels of TGF-beta1 mRNA was decreased more in the cultured mesangial cells treated with ribbon-type antisense ODN than in that of a linear-type antisense ODN for TGF-beta1. TGF-beta1 mRNA was increased markedly in the interstitium of untreated obstructed kidneys. Northem analysis revealed that the levels of TGF-beta1 mRNA were decreased in the obstructed kidneys treated with antisense ODN. The fibrosis of the obstructed kidneys treated with ribbon-type antisense ODN was dramatically less than that of the untreated group.
CONCLUSIONS
These results demonstrate that the introduction of new ribbon-type antisense ODN for TGF-beta1 may be a potential therapeutic maneuver for preventing interstitial fibrosis.

Role of Angiogenesis and Expression of Vascular Endothelial Growth Factor in Mouse Skin Carcinogenesis .: Aeree Kim, Byoung Kook Kim, Hosu Chun, Ju Han Lee, Jong Sang Choi; Korean J Pathol. 2002;36(2):106-111.

1,606 View
14 Download

Abstract PDF: BACKGROUND
Angiogenesis is crucial for many biological processes such as embryogenesis, cyclic changes in the endometrium and wound healing. It is also critical for the growth, invasion and metastasis of solid tumors. Vascular endothelial growth factor (VEGF) acts as a mitogen for endothelial cells and is expressed by the presence of various tumor cells. The objective of this study is to evaluate if angiogenesis is involved in the mouse skin carcinogenesis and if VEGF is related to angiogenesis.
METHODS
We induced premalignant and malignant lesions on mouse (BALB/c) skin using the two stage chemical carcinogenesis moedl, DMBA (7,12-dimethylbenzanthracene) initiation and TPA (tetra decanoyl-phorbol-acetate) promotion. And we analysed the microvessel densities (MVD) and expression of VEGF in various stages of premalignant and malignant lesions by immunohistochemical studies.
RESULTS
Squamous papillomas, keratoacanthoma, dermatofibroma, and squamous cell carcinomas were developed in 20 weeks. There were no differences in the incidence of benign and malignant tumors between 10-week and 20-week promotion groups. There were significant increases in MVD from normal and hyperplastic skin through premalignant lesion to invasive squamous cell carcinoma (p<0.0005). But the degree of VEGF expression neither correlated with neither MVD nor the tumor groups.
CONCLUSIONS
Increased angiogenesis begins from the hyperplastic stage. VEGF produced by tumor cells may not play major roles in the angiogenesis in the two stage chemical carcinogenesis model of the mouse skin.

First
Prev
Page of 1
Next
Last

Search