Participation of alpha-smooth muscle actin-positive cells in renomedullary interstitial cell tumors.
Renomedullary interstitial cell tumors are benign lesions which are generally discovered in specimens nephrectomized for other malignant tumors or by autopsy. We examined the histologic features of eight tumors from four patients and investigated the appearance of alpha-smooth muscle actin (ASMA)-positive cells in these tumors using immunohistochemistry. We considered that five tumors are cellular type and the remaining three as fibrous. Characteristic hyalinization was observed in two of the three fibrous tumors. All the tumors except for one fibrous type contained entrapped tubular cells. CD35-positive cells (dendritic cells) and ASMA-positive cells were observed in all the tumors, with a more frequent occurrence in the cellular type than the fibrous type. CD35-negative spindle cells were considered as fibroblasts or activated fibroblasts (myofibroblasts). The number of CD35-positive cells was higher than that of ASMA-positive cells. Additionally, the entrapped tubular cells showed the transition to spindle cells and some of them expressed for ASMA. With double immunohistochemical staining, there were some cells showing positive reactions for both CD35 and ASMA. Furthermore, an ultrastructural examination confirmed the presence of ASMA-positive filaments in the dendritic cells and myofibroblasts. The expression of TGF-beta 1 was observed not only in the tumor cells and the collecting ducts surrounding the tumor but also in the entrapped tubular cells. In addition, the intensity of TGF-beta 1 was stronger in/around the tumor than in the areas distant from the tumor. The positive cells were more numerous in the cellular type than in the fibrous type. In conclusion, ASMA-positive cells appear in renomedullary interstitial cell tumors and some of the cells may originate in dendritic interstitial cells, fibroblasts including myofibroblasts, and entrapped tubular cells. Furthermore, TGF-beta 1 may contribute to the formation of fibrosis in the tumors.
Kuroda
Naoto
N
First Department of Pathology, Kochi Medical School, Kohasu, Oko-cho, Nankoku City, Kochi 783-8505, Japan. nkuroda@kochi-ms.ac.jp
Toi
Makoto
M
Miyazaki
Eriko
E
Hayashi
Yoshihiro
Y
Nakayama
Hirofumi
H
Hiroi
Makoto
M
Enzan
Hideaki
H
D000199:Actins / Q000378:metabolism*; D000328:Adult; D000368:Aged; D005260:Female; D005350:Fibroma / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007124:Immunoenzyme Techniques; D007679:Kidney Medulla / Q000378:metabolism* / Q000473:pathology; D007680:Kidney Neoplasms / Q000378:metabolism* / Q000473:pathology / Q000648:ultrastructure; D008297:Male; D008875:Middle Aged; D009130:Muscle, Smooth / Q000378:metabolism* / Q000473:pathology; D017463:Receptors, Complement 3b / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism; D053773:Transforming Growth Factor beta1
D000199:Actins; D017463:Receptors, Complement 3b; C508960:TGFB1 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1