Mesenchymal renal tumors in F-344 newborn rats were induced by a single dose of dimethylnitrosamine. The induced tumors were successfully transplanted into adult rats under the renal capsule. Neither the primary nor the transplanted neoplasms from various generations of grafts changed their morphological features during the tumor passage, having the same cellularity with high mitotic activity and the tendency to invade the host kidney rapidly. On the basis of lectin histochemistry and immunohistology, the tumor proved to be a mesenchymal neoplasm without any obvious capacity of the proliferating cells to differentiate into any well-known organoid element normally found in mature renal parenchyma. However, the proliferating neoplastic cells were found to have a strong vimentin positivity with desmin expression. Ultrastructurally, myofilaments with attachment bodies characteristic of smooth muscle cells were generally present in various amounts in many tumor cells. In addition, on the basis of the physiological data and on kidney/tumor renin activity obtained, it is interesting to note that the tumor-graft-invaded kidneys retained their enzyme activity, despite the obvious loss of renal tissue including glomeruli. However, the immunohistochemical findings with anti-renin antibody have clearly shown that this is not due to a renin-producing tumor but rather to the surviving (probably) non-neoplastic arterioles retaining the capacity to produce renin. Although these arterioles have mostly been found next to necrotic areas, commonly occurring in dimethylnitrosamine-induced transplantable renal tumors, the question of a possible physiological role of renin in tumor necrosis or in angiogenesis has remained open.
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Adv Sci (Weinh)
January 2025
Department of Orthopaedics, The First Affiliated Hospital of Nanjing Medical University, Jiangsu, 210029, China.
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Department of Neurosurgery, University of California, Los Angeles, CA, USA.
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View Article and Find Full Text PDFTransl Androl Urol
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Department of Urology, Peking University People's Hospital, Beijing, China.
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Department of Internal Medicine, College of Medicine, Seoul National University, Seoul 03080, Korea.
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View Article and Find Full Text PDFBiomed Pharmacother
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Research Center of Integrated Traditional Chinese and Western Medicine, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou 646000, China; Institute of Integrated Chinese and Western Medicine, Southwest Medical University, Luzhou 646000, China; Institute of Integrated Chinese and Western Medicine, Southwest Medical University, Luzhou 646000, China. Electronic address:
The interaction between renal intrinsic cells and macrophages plays a crucial role in the onset and progression of kidney diseases. In recent years, epigenetic mechanisms such as DNA methylation, histone modification, and non-coding RNA regulation have become essential windows for understanding these processes. This review focuses on how renal intrinsic cells (including tubular epithelial cells, podocytes, and endothelial cells), renal cancer cells, and mesenchymal stem cells influence the function and polarization status of macrophages through their own epigenetic alterations, and how the epigenetic regulation of macrophages themselves responds to kidney damage, thus participating in renal inflammation, fibrosis, and repair.
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