Journal of Pathology and Translational Medicine

Original Articles

eNOS Gene Polymorphisms in Perinatal Hypoxic-Ischemic Encephalopathy.: Min Cho, Kwang Sun Hyun, David Chanwook Chung, In Young Choi, Myeung Ju Kim, Young Pyo Chang; Korean J Pathol. 2009;43(4):306-311.; DOI: https://doi.org/10.4132/KoreanJPathol.2009.43.4.306; Retraction in: J Pathol Transl Med 2019;53(5):345

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A Scanning Electron Microscopic Study on Microvascular Changes in the Monocrotaline-induced Rat Lung by Corrosion Casting Method.: Na Hye Myong, Eui Keun Ham; Korean J Pathol. 1995;29(5):644-659.

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Abstract: To investigate the microvascular changes in primary pulmonary hypertension, the lungs of 24 Sprague-Dawley rats were treated by an intraperitoneal injection of 2% monocrotaline(MCT) solution and then examined with scanning electron microscopy(SEM) after microvascular corrosion casting. Histologic examination revealed significant medial thickening in the small to medium-sized pulmonary arteries. Scanning electron microscopic findings of the normal lungs showed two kinds of microvascular structures. One showed a well-fortned three-dimensional basket structure of uniform flat-tubular alveolar capillaries, which were connected to each other in a T or Y shape or at right angles. The other revealed a two-dimensional reticular sheet of round tubular branches mainly in the bronchial artery-supplying regions. The MCT-treated groups(remodelling) showed apparent changes in both kinds of microvasculatures in comparison to the normal group but the more prominent change was found in Lbe bronchial artery microvasculature showing the dense thick encasement around large pulmonary arteries. Alveolar microvasculature of the pulmonary artery revealed individually enlarged angular appearance, with generally deformed alveolar architecture. Quantitatively, the significant enlargement of diameter and intercapillary distance appeared in both microvasculatures of MCT-induced rat lungs, but the density was increased only in the bronchial artery microvasculature. In conclusion, our three-dimensional microvascular study of the MCT-treated rat lungs demonstrates a new morphologic finding of vascular remodeling in primary puhnonary hypertension, which is thought to play an important vascular role in the pathogenesis in addition to interstitial fibrosis.

Expression of TGF-beta and PDGF in Monocrotaline-Induced Pulmonary Hypertension in Rats.: Min Sun Cho, Sang Ho Cho, Woo Ick Yang, Woon Sup Han; Korean J Pathol. 1999;33(8):545-554.

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Abstract PDF: Pulmonary vascular hypertension is characterized by migration and proliferation of smooth muscle cells accompanying abnormal synthesis and accumulation of extracellular proteins in vascular wall. The aim of this study is to define the role of endogneous TGF-betas and PDGF in the process of remodeling vessels through determining the temporal and spatial distribution of these growth factors in hypertensive pulmonary vessels in monocrotaline-induced pulmonary hypertension in rat. Sprague-Dawley rats were sacrificed 12 hours, 1, 2, 4, 7, 10, 14, 21, 28, and 56 days after treatment. The morphometric analysis of medial thickening and immunohistochemical study using antibodies to TGF-beta1, TGF-beta2, TGF-beta3, and PDGF were performed. Immunoreactivities for TGF-beta1 and TGF-beta3 were increased from the 14th day in the medial smooth muscle cells and PDGF showed increased expression from the 21st day in the medial smooth muscle cells. No difference in TGF-beta2 immunoreactivity was found between control and experimental groups. The expression of TGF-beta1, TGF-beta3 and PDGF increased in medial layers with the progressive thickening of pulmonary arteries which was considered to have close relation to medial hypertrophy of pulmonary arterioles. In the case of PDGF, however, the morphologic change occurred before increase in immunoreactivity was observed in the medial layer of pulmonary arterioles. Moreover, the function of isoforms of TGF-beta has yet to be completely elucidated; the different affinity to receptors and the degree of expression of these receptors that are supposed to affect the function of growth factors. Thus, further studies are needed.

A Morphological Study of the Pulmonary Endothelium and Neuroendocrine Cells in Monocrotaline-Induced Pulmonary Arterial Hypertension.: Woo Ick Yang, Sang Ho Cho, In Joon Choi, Yoo Bock Lee; Korean J Pathol. 1992;26(6):582-592.

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Abstract PDF: To investigate the mechanism of monocrotaline-induced pulmonary arterial hypertension, authors performed immunohistochemical study using antibody to von Willebrand factor(vWF), cell kinetic study using 5-bromodeoxyuridine and ultrastructural study after single subcutaneous injection of monocrotaline(MCT) to Wistar rats. The results of this study demonstrated that the expression of vWF by pulmonary endothelial cells was markedly increased from day 3 until 2 months after MCT injection. The labeling index of pulmonary microvessel endothelium began to increase after six days and was maximal on the third weeks, and thereafter it remained slightly increased above basal level. Electron microscopic study revealed attachment of inflammatory cells an platelets to endothelium from 6 hours and degranulation of attached platelets 24 hours after MCT injection. Evidences of endothelial injury began to appear from 12 hours after MCT injection. Evidences of endothelial injury began to appear from 12 hours and was maximal after 48 hours. From the third day, ultrastructural change of cell regeneration and hypertrophy began to appear and was continuosly observed until 2 months. In addition, we evaluated the changes in the number of pulmonary neuroendocrine cells using antibody to gastrin releasing peptide but it demonstrated no change until 2 months suggesting no role of neuroendocrine cells in the development of pulmonary hypertension of Wistar rats at early stage. In conclusion, the results indicate that pulmonary hypertension by MCT injection is due to increased vascular resistance caused by vasoconstriction and hyperplasia of endothelium with musculariz ation of the pulmonary arterioles induced by endothelial dysfunction and some biologic substances released form endothelium and platelets.

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