Histology and histopathology Vol.35, nº6 (2020)

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Open Access
The role of mitochondrial fusion and fission in the process of cardiac oxidative stress
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Yu, Fei; Abdelwahid, Eltyeb; Xu, Tao; Hu, Longgang; Wang, Man; Li, Yuzhen; Mogharbel, Bassam Felipe; Teixeira de Carvalho, Katherine Athayde; Guarita-Souza, Luiz Cesar; An, Yi; Li, Peifng
Summary. Mitochondria are the energy suppliers in the cell and undergo constant fusion and fission to meet metabolic demand during the cell life cycle. Well- balanced mitochondrial dynamics are extremely important and necessary for cell survival as well as for tissue homeostasis. Cardiomyocytes contain large numbers of mitochondria to satisfy the high energy demand. It has been established that deregulated processes of mitochondrial dynamics play a major role in myocardial cell death. Currently, cardiac mitochondrial cell death pathways attract great attention in the cell biology and regenerative medicine fields. Importantly, mitochondrial dynamics are tightly linked to oxidative stress-induced cardiac damage. This review summarizes molecular mechanisms of mitochondrial fusion and fission processes and their potential roles in myocardial cell death triggered by oxidative stress. Advances in understanding the effect of both normal and abnormal mitochondrial dynamics on heart protection will lead to significant improvement of therapeutic discoveries
Open Access
Overexpression of EIF5A2 is associated with poor survival and aggressive tumor biology in gallbladder cancer
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Zheng, Xin; Gao, Lei; Wang, Bo-tao; Shen, Ping; Yuan, Xiang-fei; Zhang, Lan-Qiu; Yang, Lei; Zhang, Da-Peng; Zhang, Qi; Wang, Xi-Mo
Gallbladder cancer (GBC) is a malignant tumor of the biliary tract. The main problem affecting the treatment of gallbladder cancer is late diagnosis and poor prognosis. EIF5A2 is one of two isoforms of the EIF5A family and is reported to be a new oncogenic protein in many human cancers. In this study, our results showed for the first time that EIF5A2 was overexpressed in GBC samples compared with non-tumor tissue. Overexpression of EIF5A2 was associated with lymph node metastasis, tumor differentiation, UICC (Union for International Cancer Control) staging, histological type, metastasis, and tumor size. Overexpression of EIF5A2 in gallbladder carcinoma tissues is also associated with poor prognosis in patients. The interference of EIF5A2 significantly inhibited the proliferation, cell cycle, migration and colony formation of GBC-SD cells in vitro. Our results suggest that EIF5A2 is a target oncogene and may be an important prognostic biomarker in the pathogenesis of gallbladder cancer.
Open Access
The relationship between members of the canonical NF-kB pathway, tumour microenvironment and cancer specific survival in colorectal cancer patients
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Quinn, Jean A; Bennett, Lindsay; Patel, Meera; Frixou, Mikaela; Park, James H.; Roseweir, Antonia; Horgan, Paul G; McMillan, Donald C; Edwards, Joanne
Background. The aim of this study was to investigate the role of the upstream kinase TAK1 and the canonical NF-κB pathway in colorectal cancer (CRC). Immunohistochemistry was used to assess the expression of TAK1/pTAK1 and canonical NF-κB pathway members in a tissue microarray of 242 patients. The relationship between expression, the tumour microenvironment and cancer-specific survival were examined. Results. All the investigated members of the pathway were expressed in CRC tissue. In addition, cytoplasmic pTAK1 was associated with the tumour microenvironment (P=0.045) and cancer- specific survival (CSS) (P=0.032). When cytoplasmic pTAK1 was stratified by BRAF status, cytoplasmic pTAK1 expression association with CSS was strengthened (P=0.014). Cytoplasmic IKKβ was significantly associated with the inflammatory cell infiltrate (P=0.015) as graded by Klintrup Makinen grade, systemic inflammation as assessed by neutrophil- lymphocyte ratio (P=0.03) and CSS (P=0.046). On multivariate analysis cytoplasmic IKKβ was independently associated with CSS (HR 1.75,95%CI 1.05-2.91, P=0.033). Conclusion. Cytoplasmic pTAK1 was significantly associated with CSS and this was enhanced in patients with tumours that expressed wild type BRAF. High expression of cytoplasmic IKKβ was significantly associated with decreased CSS and with markers of the tumour microenvironment. These results support the hypothesis that NF-κB pathway members are poor prognostic markers in patients with CRC, but this requires to be validated in a large independent cohort
Open Access
Pyloric and foveolar type metaplasia are important diagnostic features in Crohn’s disease that are frequently missed in routine pathology
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Meditskou, Soultana; Grekou, Alexandra; Toskas, Alexandros; Papamitsou, Theodora; Miliaras, Dimosthenis
Pyloric type metaplasia (PYME) as evidence of chronic mucosal damage, is one of the main histopathological findings for diagnosing Crohn’s Disease (CD) in terminal ileum biopsies, according to the latest guidelines but still frequently underdiagnosed in routine pathology. Foveolar metaplasia (FOME) changes in mucosa, another aspect of the chronic post - inflammatory Ulcer Associated Cell Lineage (UACL), have only been reported in a few cases. However, their clinical significance has not been investigated in depth except in pouchitis. The aim of this study was to investigate the importance of meticulous study of terminal ileum biopsies for the recognition of PYME/FOME as an adjunct finding helpful for the diagnosis of CD. In the present study, two experienced gastrointestinal pathologists, have reviewed 105 terminal ileum biopsies from 105 patients with CD, using a protocol of 15 sections on average per biopsy. In 21% (22/105) of cases PYME was recognized and in 4% (4/105) FOME was also present. PYME/FOME had not been detected in 83% of these cases in the original reports. FOME was also identified in terminal ileum biopsies, a feature not reported previously in CD. Conclusively, PYME/FOME can be easily missed in terminal ileum biopsies from patients with suspected or known CD unless a meticulous study of the histologic material is carried out combined with awareness of the pathologist about its importance.
Open Access
Aliskiren improves renal morphophysiology and inflammation in Wistar rats with 2K1C renovascular hypertension
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Pereira, Priscila G.; Rabelo, Kíssila; Silva da, Jemima F. R.; Ciambarella, Bianca T.; Argento, Juliana G.C.; Nascimento, Ana L.R.; Vieira, Aline B.; Carvalho de, Jorge J.
Hypertension is characterized by persistent elevated blood pressure levels, one of the leading causes of death in the world. Renovascular hypertension represents the most common cause of secondary hypertension, and its progress is associated with overactivation of the renin angiotensin aldosterone system (RAAS), causing systemic and local changes. Aliskiren is a renin-inhibiting drug that optimizes RAAS suppression. In this sense, the objective of the present study was to analyze the morphophysiology of the left kidney in Wistar rats with renovascular hypertension after treatment with Aliskiren. Parameters such as systolic blood pressure, urinary creatinine and protein excretion, renal cortex structure and ultrastructure, fibrosis and tissue inflammation were analyzed. Our results showed that the hypertensive animals treated with Aliskiren presented a reestablishment of blood pressure, expression of renin, and renal function, as well as a remodeling of morphological alterations through the reduction of fibrosis. The treatment regulated the laminin expression and decreased pro-inflammatory cytokines, restoring the integrity of the glomerular filtration barrier. Therefore, our findings suggest that Aliskiren has a renoprotective effect acting on the improvement of the morphology, physiology and pathology of the renal cortex of animals with renovascular hypertension
Open Access
Bovine oviduct epithelial cells suppress the phagocytic activity of neutrophils towards sperm but not for bacteria in vitro: Immunofluorescence and electron microscopic observations
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Marey, Mohamed Ali; Matsukawa, Haruhisa; Sasaki, Motoki; Ezz, Mohamed Aboul; Yousef, Mohamed Samy; Takahashi, Ken-ichi; Miyamoto, Akio
Previously, we reported that polymorpho- nuclear neutrophils (PMNs) are constantly existent in the bovine oviduct fluid during the pre-ovulatory stage under physiological conditions. Moreover, incubation of PMNs with bovine oviduct epithelial cells-conditioned medium (BOEC-CM) resulted in suppression of their phagocytic activity for sperm. During pathophysiological conditions, cows may be inseminated by infected semen which exposes oviductal PMNs to allogenic sperm simultaneously with pathogens. This study aimed to visually investigate the role of oviduct epithelium in regulating the phagocytic behavior of PMNs toward sperm as a physiological stimulus, with Escherichia coli (E. coli) as a pathological stimulus. In our experiment, PMNs were incubated for 2 h in BOEC-CM. Phagocytosis was then assayed by co-incubation of these PMNs either with sperm, E. coli, or latex beads. BOEC- CM significantly suppressed the direct phagocytosis of PMNs for sperm, but did not affect their phagocytic activity for E. coli or latex beads. Additionally, an investigation with scanning electron microscopy revealed that BOEC-CM suppressed the formation of DNA-based neutrophil extracellular traps (NETs) for sperm entanglement. BOEC-CM did not alter NETs formation towards E. coli. A quantification of NETs formation using an immunofluorescence microscopy showed that the areas of NETs formation for E. coli were significantly larger than those formed for sperm. Our data clearly show that the bovine oviduct, through secretions, protects sperm from phagocytosis by PMNs and eliminates bacterial dissemination through maintaining the phagocytic activity of PMNs towards bacteria
Open Access
Expression of glucose-regulated protein 78 as prognostic biomarker for triple-negative breast cancer
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Yang, Chenlian; Zhang, Zhiwei; Zou, Yutian; Gao, Guanfeng; Liu, Lingrui; Xu, Haifan; Liu, Feng
Introduction. glucose-regulated protein78 (GRP78) is a stress - induced endoplasmic reticulum chaperone protein. It is closely related to the occurrence, development, proliferation, differentiation and drug resistance of breast cancer. However, the association and clinicopathological features between GRP78 and triple negative breast cancer (TNBC) remain to be studied. Material and Methods. Clinical and pathological characteristics and overall survival were analysed retrospectively in 179 surgically resected TNBC patients. GRP78 was detected by immunohistochemistry (IHC) using breast cancer tissue microarrays (TMAs), and the association between GRP78 levels and clinicopathological factors and prognosis was analyzed. Furthermore, GRP78 expression in human TNBC and NTNBC cell lines was detected by Western blot and qRT-PCR. After Si-GRP78 knocked-down GRP78 in MDA-MB-231 and BT549 cell lines, cell proliferation was detected using Cell Counting Kit-8 (CCK-8) and cell colony formation was detected by crystal violet staining, respectively. Results. GRP78 was expressed in triple negative breast cancer (TNBC). GRP78 expression was significantly associated with invasive, distant metastasis and proliferation of TNBC (P<0.05). In addition, patients with positive GRP78 expression had shorter overall survival (OS) and disease-free survival (DFS). And the high expression of GRP78 was significantly associated with disease-free survival (DFS) in patients with TNBC (P<0.001). Conclusions. These findings improve our understanding of the expression pattern of GRP78 in TNBC and clarify the role of GRP78 as a promising prognostic biomarker for triple-negative breast cancer.
Open Access
How galectins have become multifunctional proteins
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) García Caballero, Gabriel; Kaltner, Herbert; Kutzner, Tanja J.; Ludwig, Anna-Kristin; Manning, Joachim C.; Schmidt, Sebastian; Sinowatz, Fred; Gabius, Hans-Joachim
Having identified glycans of cellular glycoconjugates as versatile molecular messages, their recognition by sugar receptors (lectins) is a fundamental mechanism within the flow of biological information. This type of molecular interplay is increasingly revealed to be involved in a wide range of (patho)physiological processes. To do so, it is a vital prerequisite that a lectin (and its expression) can develop more than a single skill, that is the general ability to bind glycans. By studying the example of vertebrate galectins as a model, a total of five relevant characteristics is disclosed: i) access to intra- and extracellular sites, ii) fine-tuned gene regulation (with evidence for co-regulation of counterreceptors) including the existence of variants due to alternative splicing or single nucleotide polymorphisms, iii) specificity to distinct glycans from the glycome with different molecular meaning, iv) binding capacity also to peptide motifs at different sites on the protein and v) diversity of modular architecture. They combine to endow these lectins with the capacity to serve as multi-purpose tools. Underscoring the arising broad-scale significance of tissue lectins, their numbers in terms of known families and group members have steadily grown by respective research that therefore unveiled a well-stocked toolbox. The generation of a network of (ga)lectins by evolutionary diversification affords the opportunity for additive/synergistic or antagonistic interplay in situ, an emerging aspect of (ga)lectin functionality. It warrants close scrutiny. The realization of the enormous potential of combinatorial permutations using the five listed features gives further efforts to understand the rules of functional glycomics/lectinomics a clear direction.
Open Access
Triptolide inhibits tonsillar IgA production by upregulating FDC-SP in IgA nephropathy
(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Li, Huining; Yang, Xinxin; Yao, Guodong; Zhang, Yanxiang; Xu, Yangyang; Cao, Yan; An, Xushu; Li, Haibo; Chen, Hui; Geng, Jingshu; Yuan, Dawei; Jin, Xiaoming; Meng, Hongxue
IgA nephropathy (IgAN) is primarily resulted of qualitative abnormality of IgA. The occurrence of IgAN is associated with affected tonsils which enhances the IgA production via IgA class switching and immuno-activation. Follicular dendritic cell-secreted protein (FDC-SP) was found to be a negative effect for IgA production in tonsil. The previous studies suggested that Triptolide might reduce IgA production by its immunosuppression role. Given this background, this study investigated the mechanisms underlying the role of Triptolide and FDC-SP in the generation of IgA and IgA class switching in tonsil of IgAN patients. Immunohistochemistry and reverse transcription-polymerase chain reaction revealed that the expression of FDC-SP was increased in the tonsils of IgAN patients with Triptolide treatment compared with those without treatment. Meanwhile, the expression of FDC-SP was negatively correlated with IgA inducing cytokines in the tonsils of IgAN patients treated with Triptolide, due to the significant decreased IgA-bearing cells. The expression of FDC-SP in tonsillar tissue was confirmed by double immunofluorescence. Importantly, Triptolide promoted FDC-SP secretion, and correlated negatively with decreased IgA production in isolated FDC-associated clusters, which had been isolated from patients without TW treatment previously. Our study demonstrated that Triptolide might have an impact on FDC-SP production and downregulation of IgA synthesis in the tonsils of IgAN patients, which could be a promising strategy for therapeutic intervention in IgAN patients.

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