Histology and histopathology Vol.33, nº7 (2018)

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Open Access
Low-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, Jenneke
Disturbed 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.
Open Access
Leishmania 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, Tânia
Leishmania 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.
Open Access
Elevated cathepsin K potentiates metastasis of epithelial ovarian cancer
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Fan, Xiujie; Wang, Chongjuan; Song, Xianhui; Liu, Huaqing; Li, Xue; Zhang, Yuanfang
Cathepsin K, or CTSK, has been found to be involved in the peritoneal metastasis of ovarian carcinoma. However, the expression and clinicopathological significance of CTSK remains unknown in epithelial ovarian cancer (EOC). The aim of the present study was to investigate the expression of CTSK and its clinicopathological significance in EOC. TSK expression was evaluated using immunohistochemistry in EOC tissue microarray. The expression of CTSK in EOC was displayed to be markedly higher than that of adjacent normal control. In addition, CSTK expression was shown to be remarkably associated with metastases and inferior overall prognosis of EOC. In vitro, Knock-down of CTSD was exhibited to be able to suppress migration and invasion in EOC cell lines OV2008 but not proliferation in OV-2008. Together, our data showed that elevated CTSD in EOC can potentiate the metastasis of EOC cells, suggesting that targeting CTSD might be used as a novel therapeutic target for EOC.
Open Access
Down-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 Chuan
REIC (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.
Open Access
Current status of bone regeneration using adipose-derived stem cells
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Tajima, Satoshi; Tobita, Morikuni; Mizuno, Hiroshi
Many bone regeneration therapies have been developed for clinical use and have variable outcomes and serious limitations. The goal of bone regeneration is to repair a bone defect in a stable and durable manner. Cellular strategies play an important role in bone tissue engineering. Clinical factors important for successful bone regeneration are the recruitment of cells to the defect site and the production of a suitable extracellular matrix consistent with bone tissues. Adipose-derived stem cells (ASCs) can be obtained in large quantities with little donor site morbidity or patient discomfort. They are multipotent somatic stem cells and have a strong potential to differentiate and secrete growth factors. In this review, we discuss the osteogenic potential of ASCs with/without several types of scaffolds in vivo and their clinical application for bone regeneration.
Open Access
Adipose-derived stem cells in articular cartilage regeneration: current concepts and optimization strategies
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Gu, Xingjian; Li, Caixin; Yin, Feng; Yang, Guanghua
Knee osteoarthritis (KOA) is the most common progressive joint disorder associated with disability in the world. As a chronic disease, KOA has multifactorial etiology. However, the poor self-healing ability of the articular cartilage due to its intrinsic tissue hypovascularity and hypocellularity seems to be directly incriminated in the physio-pathological mechanism of KOA. While conventional therapies result in unfavorable clinical outcomes, regenerative cell therapies have shown great promise in articular cartilage regeneration. Adipose-derived stem cells (ASCs) appear to be an ideal alternative to bone-marrow derived stem cells (BMSCs) and autologous chondrocytes, due to their lower immunogenicity, richer source and easier acquisition. Since the first case report in 2011, ASCs have demonstrated safety and efficacy for articular cartilage regeneration in several phase I/II clinical trials. However, different levels of abnormality were found in the regenerated cartilage for most of the patients. A large portion of recent publications investigated different optimization strategies to improve the therapeutic function of ASCs, including cell source selection, preconditioning and co-delivery. Herein, we give an update on the latest research progress on ASCs, with a focus on the most promising optimization strategies for ASC-based therapy.
Open Access
Ageing-related aorta remodelling and calcification occur earlier and progress more severely in rats with spontaneous hypertension
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Shi, Xiaoyun; Bai, Yajing; Ke, Yilang; Chen, Ruiqi; Lin, Xiaohong; Chen, Lianglong; Hong, Huashan
The effects of hypertension on vascular remodelling, ageing and calcification are not fully understood. In this study, we monitored the dynamic changes of aorta remodelling, senescence and calcification in spontaneously hypertensive rats (SHRs) during ageing. Results. Vascular remodelling and senescence cells occurred in SHR aortas at 24 weeks. The calcium content and calcium deposition of the aorta increased in SHRs at 48 weeks. All of these changes became increasingly significant with ageing. In contrast, these pathologic changes appeared in Wistar-Kyoto (WKY) normotensive rats at a much later stage (72 weeks). These data showed that the ageing-related aorta remodelling, senescence and calcification in SHRs occurred earlier and progressed more severely than in WKY rats. Conclusion. Ageing-related vascular remodelling and calcification were accelerated and augmented in SHR aortas.
Open Access
Spontaneous intracerebral hemorrhage as presentation of atypical central neurocytoma: the role of angiogenesis through the characterization of tumor endothelial cells
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Marfia, Giovanni; Pirola, Elena; Navone, Stefania Elena; Beretta, Matteo; Guarnaccia, Laura; Trombetta, Elena; Franzini, Andrea; Rampini, Paolo; Campanella, Rolando
A 36-year-old white man presented with sudden-onset headache and rapid deterioration of consciousness. Computer tomography revealed a right capsular intra-parenchimal hemorrhage with an intraventricular component; therefore, emergency surgery was performed. Once the hematoma was evacuated, the cause of the hemorrhage was identified as a tumor mass and it was resected. Histopathological and immunohistochemical examinations of the surgical specimen disclosed a diagnosis of atypical central neurocytoma. By using a protocol recently set up in our laboratory, we succeeded in isolating and propagating, for the first time, human endothelial cells from central neurocytoma (CN-ECs). Different analyses revealed that isolated CNECs consist of a pure endothelial cell population, with the expression of endothelial markers (CD31, CD309/VEGFR2, CD105, eNOS) and with angiogenic properties, such as the uptake of LDL. Moreover, CNECs spontaneously organize in a vascular-like structure. The goal of this case report is to stress the need for further studies focused on understanding the causes of the onset of an intra-parenchimal hemorrhage in the presence of an atypical central neurocytoma in order to tailor treatments to each single patient and achieve the best clinical outcome.
Open Access
Killing two birds with one stone: The multifunctional roles of mesenchymal stem cells in the treatment of neurodegenerative and muscle diseases
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Lee, Na Kyung; Na, Duk L.; Chang, Jong Wook
Neurodegenerative and muscle diseases bear both complex and multifactorial pathologies. An efficacious and robust therapeutic option to treat these diseases is yet to be elucidated. At such a time, mesenchymal stem cells have drawn significant attention due to their immunomodulatory and regenerative properties. Accumulating evidence has proposed the capability of MSCs to serve multiple roles in a broad spectrum of diseases by secretion of trophic or paracrine factors. In the present review, we will look into the recent literature and discuss the therapeutic functions of MSCs and their potential to treat various neurodegenerative (Alzheimer’s, Parkinson’s, and Huntington’s disease) and muscle (Duchenne muscular dystrophy, myopathy, and multiple sclerosis) diseases.
Open Access
Distinctive 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, Anna
The 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.
Open Access
Autophagy 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, Qiang
Proteinuria (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.
Open Access
Potential role of NDRG2 in reprogramming cancer metabolism and epithelial-to-mesenchymal transition
(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Chen, Xiang Liu; Lei, Lan; Hong, Lian Lian; Ling, Zhi Qiang
Epithelial-to-mesenchymal transition (EMT) allows a cell with epithelial characteristics to transdifferentiate into a cell with mesenchymal characteristics, which is recognized as a key priming event for the initiation and evolvement of cancer metastasis. Accumulating data has shown that aberrant cancer metabolism contributes to the execution of EMT and cancer metastasis through multiple pathological pathways. Recently, the N-MYC downstream-regulated gene 2 (NDRG2), as a tumor suppressor and metabolism-related gene in various cancers, has been widely noted. NDGR2 is associated with energy metabolism, especially glycose metabolism. Hence, we propose a hypothesis that EMT is repressed by NDRG2 via cancer metabolic reprogramming, and summarize the pathological processes and molecular pathways related to the regulation of NDRG2.

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