Histology and histopathology Vol.33, nº7 (2018)
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- PublicationOpen AccessAutophagy activation promotes removal of damaged mitochondria and protects against renal tubular injury induced by albumin overload(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Tan, Jin; Wang, Miaohong; Song, Shuling; Miao, Yuyang; Zhang, QiangProteinuria (albuminuria) is an important cause of aggravating tubulointerstitial injury. Previous studies have shown that autophagy activation can alleviate renal tubular epithelial cell injury caused by urinary protein, but the mechanism is not clear. Here, we investigated the role of clearance of damaged mitochondria in this protective effect. We found that albumin overload induces a significant increase in turnover of LC3-II and decrease in p62 protein level in renal proximal tubular (HK-2) cells in vitro. Albumin overload also induces an increase in mitochondrial damage. ALC, a mitochondrial torpent, alleviates mitochondrial damage induced by albumin overload and also decreases autophagy, while mitochondrial damage revulsant CCCP further increases autophagy. Furthermore, pretreatment of HK-2 cells with rapamycin reduced the amount of damaged mitochondria and the level of apoptosis induced by albumin overload. In contrast, blocking autophagy with chloroquine exerted an opposite effect. Taken together, our results indicated autophagy activation promotes removal of damaged mitochondria and protects against renal tubular injury caused by albumin overload. This further confirms previous research that autophagy activation is an adaptive response in renal tubular epithelial cells after urinary protein overload.
- PublicationOpen AccessLeishmania amazonensis isolated from human visceral leishmaniasis: histopathological analysis and parasitological burden in different inbred mice(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Freitas de Souza, Celeste da Silva; Calabrese, Kátia da Silva; Abreu Silva, Ana Lúcia; Pereira Carvalho, Luiz Otávio; de Oliveira Cardoso, Flávia; Moraes Cavalheiros Dorval, Maria Elizabeth; Teruya Oshiro, Elisa; Quaresma, Patrícia Flávia; Ferreira Gontijo, Célia Maria; da Silva Pacheco, Raquel; Doria Rossi, Maria Isabel; Gonçalves da Costa, Sylvio Celso; Zaverucha do Valle, TâniaLeishmania amazonensis is a major etiological agent of human cutaneous leishmaniasis in the Americas; nevertheless there are some reports of this species causing visceral disease in dogs and men. In the present work we have studied a Leishmania strain isolated from a human case of visceral leishmaniasis. We have infected different mouse strains and analyzed the development of the disease, studying the parasite’s ability to visceralize and whether this ability is influenced by host genetics. Female BALB/c, C57BL/6, C57BL/10, CBA, DBA/2, and C3H/He mice were subcutaneously infected with 104 L. amazonensis amastigotes. BALB/c, C57BL/6 and C57BL/10 mice were found to be very susceptible to infection, showing lesions that developed to necrosis and ulceration. CBA mice developed a late but severe lesion. DBA/2 mice developed only discrete lesions, while C3H/He mice did not develop any lesions. All mouse strains except C3H/He showed some degree of visceralization, presenting parasites in the spleen, while BALB/c, C57BL/6 and CBA presented parasites also in the liver. Moreover, most of the strains presented high parasite load at the infection site, whereas DBA and C3H/He mice showed low or no parasite load 90 days after infection, respectively. Histopathology corroborates the results, showing that susceptible mice presented an inflammatory reaction with parasites in the skin, lymph nodes and spleen, while strains that are more resistant presented low parasitism and discrete inflammatory reaction. Results indicate that this isolate is extremely virulent, can easily visceralize and that the pathogenesis of leishmaniasis is, at least in part, related to the genetic background of the host.
- PublicationOpen AccessDistinctive peri-luminal presence of agrin in murine and human carotid atherosclerotic plaques(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Rauch, Uwe; Bengtsson, Eva; Gonçalves, Isabel; Hultgårdh Nilsson, AnnaThe clinical consequences of arterial atherosclerotic lesions depend, apart from their size, on their composition of cellular and extracellular components. While an intact endothelium at the interface of atherosclerotic plaques towards the blood can prevent its erosion, underlying smooth muscle cells within the plaque can reduce the risk of plaque ruptures, due to the deposition of stabilizing extracellular matrix. Basement membranes underlay and support the function of endothelial cells, and embed smooth muscle cells in the media, the source of most smooth muscle cells within atherosclerotic plaques. In the present study mouse atherosclerotic plaques were comparatively analyzed for the basement membrane components laminin, type IV collagen, perlecan, and agrin. Distinct agrin immunofluorescence was found in the peri-luminal area in mouse carotid atherosclerotic plaques. Agrin was also clearly present in the media, with a significant increase in regions directly associated with plaque tissue. In addition, ten human endarterectomy specimens were investigated for this heparan sulfate proteoglycan. No statistically significant differences in agrin immunofluorescence were noticed between five specimens from symptomatic and five from asymptomatic patients. In all these plaques agrin was present in a distinctive manner in a narrow zone partially or almost completely surrounding the lumen. Additionally it was also present around the small lumina of the CD31-positive neovessels. The presence of agrin at locations with particular importance for the growth and stability of atherosclerotic plaques renders this molecule strategically positioned to influence plaque development and vulnerability.
- PublicationOpen AccessLow-intensity pulsed ultrasound increased blood vessel size during fracture healing in patients with a delayed-union of the osteotomized fibula(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Korstjens, Clara M.; Rutten, Sjoerd; Nolte, Peter A.; van Duin, Marion A.; Klein Nulend, JennekeDisturbed vascularity leads to impaired fracture healing. Since low-intensity pulsed ultrasound (LIPUS) increases new bone formation in delayedunions, we investigated whether LIPUS increases blood supply in delayed-unions of the osteotomized fibula, and if LIPUS-increased bone formation is correlated to increased blood supply. Blood vessel parameters were analysed using histology, immunohistochemistry, and histomorphometric analysis as well as their correlation with bone formation and resorption parameters. Fibular biopsies of thirteen patients with a delayed-union of the osteotomized fibula treated for 2-4 months with or without LIPUS originating from a randomized prospective double-blind placebo-controlled clinical trial were studied. In histological sections of the fibular biopsies parameters of blood vessel formation were measured and were related to histomorphometric bone characteristics of newly formed bone of the same samples analysed in our previously published study on the effects of LIPUS on bone healing at the tissue level in delayed-unions. LIPUS-treated delayed-unions and sham-treated delayed-unions as well as healed delayedunions and failed-to-heal delayed-unions were compared. The volume density of blood vessels was increased in LIPUS-treated delayed-unions compared to sham-treated controls. LIPUS did not change blood vessel number, but significantly increased blood vessel size. Healed delayed-unions as well as LIPUS-treated and sham-treated delayed-unions showed significant correlations between blood vessel size and osteoid volume. LIPUS increases blood vessel size, essential for fracture healing, in bone from patients with a delayedunion of the osteotomized fibula. The increased osteoid volume in delayed-unions can largely be explained by increased blood supply and perfusion.
- PublicationOpen AccessDown-regulated REIC expression in lung carcinogenesis: a molecular target for gene therapy(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Yang, Lei; Zhao, Shuang; Xia, Pu; Zheng, Hua ChuanREIC (Reduced Expression in Immortalized Cells) gene is down-regulated in immortalized cells, compared with the normal parental counterparts. Its encoding protein could inhibit colony formation, tumor growth, and induce apoptosis. To investigate the roles of REIC expression in lung cancer, we examined REIC expression in lung cancer cells and tissues by RT-PCR or Western blot, and observed the effects of both recombinant REIC exposure and REIC overexpression on the aggressive phenotypes of lung cancer cells. It was found that the demethylation of REIC promoter by 5- Aza-dC could reserve its mRNA expression in lung cancer cells (P<0.05). There was a lower REIC mRNA expression in lung cancer than that in matched normal tissue (P<0.05). Recombinant REIC treatment enhanced the proliferation of lung cancer cells (P<0.05), but versa for REIC overexpression (P<0.05). Both recombinant REIC treatment and REIC overexpression induced apoptosis, and inhibited the migration and invasion of SQ-5 and KJ cells (P<0.05). Immunohistochemically, there was a positive correlation between REIC and Caspase-3 expression in lung cancer (P<0.05). According to Kaplan-Meier plotter, REIC mRNA overexpression was found to positively correlate with overall, progression-free and post- progression survival rates of lung cancer patients (P<0.05), even stratified by sex, histological subtyping, grading, TNM staging, chemotherapy, radiotherapy, or smoking. These findings suggested that down-regulated REIC expression might be involved in lung carcinogenesis due to its promoter methylation. Both recombinant REIC exposure and REIC overexpression might reverse the aggressive phenotypes of lung cancer cells. REIC may be employed as a potential target of gene therapy for lung cancer.
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