Histopathological, Immunohistochemical and Ultrastructural Studies of a Renal Mesenchymal Tumor in a Young Beagle Dog

Suzuki, Yui; Takaba, Katsumi; Yamaguchi, Iwao; Myoujou, Kensuke; Kimoto, Naoya; Ikegami, Hiroki; Saeki, Koji; Imaizumi, Minami; Takada, Chie

doi:10.1292/jvms.10-0504

Cited by 5 publications

(7 citation statements)

References 11 publications

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“…5,10 Most renomedullary interstitial cells express high levels of cyclooxygenase-2 (COX-2), which is the inducible isoform of prostaglandin-endoperoxide synthase 2. 5,13 In humans, renal interstitial cell tumors are known to be COX-2 positive. 10 Moreover, in humans, these mesenchymal tumors are known as renomedullary interstitial cell tumors, which are benign neoplasms diagnosed only rarely prior to death; they were previously described as medullary fibromas or hamartomas.…”

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confidence: 99%

Renal interstitial cell tumor in a dog: clinicopathologic, imaging, and histologic features

et al. 2019

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Renal interstitial cell tumors are benign tumors of renomedullary origin; however, malignant features have not been reported in dogs, to our knowledge. A 17-y-old spayed female Maltese dog was presented to a local animal hospital with a mass in the right abdomen. Clinicopathologic findings prior to surgery revealed renal insufficiency and anemia. Imaging revealed that the right kidney was enlarged by an amorphous mass with opaque areas, indicative of mineralization. Upon histologic examination, the mass was comprised of malignant mesenchymal cells that produced mucinous matrix. The tumor cells were positive for vimentin and COX-2, but negative for pancytokeratin; the matrix stained positively with alcian blue. Therefore, the mass was diagnosed as a renal interstitial cell tumor, with malignant features. COX-2 may be useful in the diagnosis of canine renal interstitial cell tumors, similar to its diagnostic role in humans.

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confidence: 99%

Renal interstitial cell tumor in a dog: clinicopathologic, imaging, and histologic features

et al. 2019

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“…Congenital mesoblastic nephroma has been previously described in a 7‐month‐old male beagle dog, in a 10‐month‐old male beagle dog and in a 15‐month‐old male beagle dog. These dogs were kept in a laboratory animal facility, were clinically healthy, and in all cases the renal mass was observed incidentally during necropsy after experimental use (Takeda and others , Yoshizawa and others , Suzuki and others ). A tumour with similar histological features, but which was diagnosed as a mixed mesenchymal tumour, has also been described in an 11‐month‐old female beagle dog used in a toxicity study (Robison and others ).…”

Section: Discussionmentioning

confidence: 99%

Congenital mesoblastic nephroma in a young basset hound dog

Soldati¹,

Radælli

Mazzuti³

et al. 2012

J of Small Animal Practice

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An 18-month-old male basset hound was presented with vomiting, diarrhoea and depression. Abdominal ultrasonography revealed a mass in the left kidney. An ultrasound-guided core-biopsy indicated aggregates of spindle cells, but did not allow a definitive diagnosis. Nephrectomy was performed after a period of six months, when ultrasound examination revealed a slight increase in mass dimensions. Histologically the mass was composed of neoplastic spindle cells forming interlacing fascicles, bundles and whorls, within a loose myxoid to dense collagenous stroma. Immunohistochemically neoplastic cells were positive for vimentin and smooth muscle actin. Based on these findings the tumour was diagnosed as a congenital mesoblastic nephroma, classical variant. After a two-and-a-half-year follow-up the dog was clinically healthy, indicating a benign behaviour. To the authors' knowledge, this report describes the first case of canine congenital mesoblastic nephroma successfully treated surgically, with a reasonable postsurgical follow-up.

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“…α‐Smooth muscle actin (α‐SMA) represents a marker of fibroblastic cells, that is, Ac‐HSCs, whereas desmin is a marker of quiescent HSC and stains many pericentral fat‐storing cells in normal rat liver . Moreover, immunohistochemical staining for α‐SMA (Dako, Kyoto, Japan) and desmin (Nichirei, Tokyo, Japan) was carried out . Stained sections were analyzed using ImageJ software (version 1.47; https://imagej.nih.gov/ij/; National Institutes of Health, Bethesda, MD, USA).…”

Section: Methodsmentioning

confidence: 99%

“…24 Moreover, immunohistochemical staining for α-SMA (Dako, Kyoto, Japan) and desmin (Nichirei, Tokyo, Japan) was carried out. [25][26][27] Stained sections were analyzed using ImageJ software (version 1.47; https://imagej.nih.gov/ij/; National Institutes of Health, Bethesda, MD, USA). Six microscopic visual fields (magnification ×40) per specimen from 10 rats were used for ImageJ analysis, as previously described.…”

Section: Histological and Immunohistochemical Analysesmentioning

confidence: 99%

Combined effect of a farnesoid X receptor agonist and dipeptidyl peptidase‐4 inhibitor on hepatic fibrosis

Shimozato

Namisaki

Kaji

et al. 2019

Hepatology Research

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Aim Non‐alcoholic steatohepatitis (NASH) has a broad clinicopathological spectrum (inflammation to severe fibrosis). The farnesoid X receptor agonist obeticholic acid (OCA) ameliorates the histological features of NASH; satisfactory antifibrotic effects have not yet been reported. Here, we investigated the combined effects of OCA + a dipeptidyl peptidase‐4 inhibitor (sitagliptin) on hepatic fibrogenesis in a rat model of NASH. Methods Fifty Fischer 344 rats were fed a choline‐deficient L‐amino‐acid‐defined (CDAA) diet for 12 weeks. The in vitro and in vivo effects of OCA + sitagliptin were assessed along with hepatic fibrogenesis, lipopolysaccharide–Toll‐like receptor 4 (TLR4) regulatory cascade and intestinal barrier function. Direct inhibitory effects of OCA + sitagliptin on activated hepatic stellate cells (Ac‐HSCs) were assessed in vitro. Results Treatment with OCA + sitagliptin potentially inhibited hepatic fibrogenesis along with Ac‐HSC proliferation and hepatic transforming growth factor (TGF)‐β1, α1(I)‐procollagen, and tissue inhibitor of metalloproteinase‐1 (TIMP‐1) mRNA expression and hydroxyproline levels. Obeticholic acid inhibited hepatic TLR4 expression and increased hepatic matrix metalloproteinase‐2 expression. Obeticholic acid decreased intestinal permeability by ameliorating CDAA diet‐induced zonula occludens‐1 disruption, whereas sitagliptin directly inhibited Ac‐HSC proliferation. The in vitro suppressive effects of OCA + sitagliptin on TGF‐β1 and α1(I)‐procollagen mRNA expression and p38 phosphorylation in Ac‐HSCs were almost consistent. Sitagliptin directly inhibited the regulation of Ac‐HSC. Conclusions Treatment with OCA + sitagliptin synergistically affected hepatic fibrogenesis by counteracting endotoxemia induced by intestinal barrier dysfunction and suppressing Ac‐HSC proliferation. Thus, OCA + sitagliptin could be a promising therapeutic strategy for NASH.

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Histopathological, Immunohistochemical and Ultrastructural Studies of a Renal Mesenchymal Tumor in a Young Beagle Dog

Cited by 5 publications

References 11 publications

Renal interstitial cell tumor in a dog: clinicopathologic, imaging, and histologic features

Renal interstitial cell tumor in a dog: clinicopathologic, imaging, and histologic features

Congenital mesoblastic nephroma in a young basset hound dog

Combined effect of a farnesoid X receptor agonist and dipeptidyl peptidase‐4 inhibitor on hepatic fibrosis

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