Spongiotic reaction patterns in autoimmune bullous dermatoses (Review)

xlomafota13 shared this article with you from Inoreader Spongiotic reaction patterns in autoimmune bullous dermatoses (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1334. doi: 10.3892/etm.2021.10769. Epub 2021 Sep 20. ABSTRACT Spongiosis or a spongiotic reaction pattern is the histological hallmark of intercellular epidermal edema, viewed as clear spaces within the epidermis. Although considered a histopathological term, spongiosis has clinical correlations, with the variable degrees of spongiotic reaction leading to different dermatological findings. This review aimed to highlight the spongiotic reactive patterns found in different autoimmune bullous dermatoses, considering the paucity of publications in this domain. The pathogenesis of spongiosis assumes the passage of extravasated edema fluid from the dermis into the epidermis, frequently accompanied by dermal inflammatory cells, and classification of the spongiotic reaction patterns, as well as their associated spongiotic dermatitis, take into consideration the type and distribution of these inflammatory cells. It is mandatory to consider different reactive processes, specific for other skin disorders, which act as simulants of different spongiotic patterns for the diagnosis. Considering the possible transient occurrence, the heterogeneity and non-specificity of the histopathological features of these diseases, the diagnosis is very complex, requiring clinicopathological correlations and additional analyses. A deep insight into spongiosis pathogeny may open the perspectives of a classification refinement of autoimmune bullous dermatoses. PMID:34630688 | PMC:PMC8495556 | DOI:10.3892/etm.2021.10769 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Predictive factors for the recurrence of surgically excised basal cell carcinomas: A retrospective clinical and immunopathological pilot study

xlomafota13 shared this article with you from Inoreader Predictive factors for the recurrence of surgically excised basal cell carcinomas: A retrospective clinical and immunopathological pilot study Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1336. doi: 10.3892/etm.2021.10771. Epub 2021 Sep 20. ABSTRACT Basal cell carcinoma (BCC) is the most frequent form of skin cancer and is not a tumor with a lethal outcome if diagnosed and treated adequately. The gold standard for treatment is surgical excision with histologically safe margins. Even so, tumors excised with free margins may recur after a period of time. The identification of predictive factors for the recurrence of BCCs besides the localization, size and aggressive histology may be useful for the clinician. The aim of the present study was to identify clinical and pathological factors associated with recurrence in tumors with histologically free margins and assess via immunohistochemical staining, the expression of glioma-associated oncogene homolog 1 (GLI1), yes-associated protein (YAP), connective tissue growth factor (CTGF) and E-cadherin as they are involved in the development of BCCs, in the hope of identifying markers that are predictive for recurrence. In total, 8 recurrent BCCs and 38 non-recurrent tumors were analyzed. A Breslow index >2 (Se 100.0%, Sp 67.5%, P=0.008), Clark level >3 (Se 100.0%, Sp 47.5%, P<0.001), and excision margins both lateral (Se 87.5%, Sp 60.0%, P=0.04) and deep (Se 75.0%, Sp 82.5%, P<0.001) free from tumoral cells ≤1 mm proved to be predictive for recurrence in the present study. Recurrence may appear even after more than 3 years since the initial excision (Se 87.50%, Sp 70.0%, P<0.001). The expression levels of GLI1, YAP and E-cadherin were not different in the recurrent vs. non-recurrent BCCs. However, the low expression of CTGF may indicate a tumor with a higher aggressiveness. In conclusion, close follow-up of patients with excised BCCs at least annually is recommended and re-excision should be taken into consideration for locally advanced tumors especially if they are located in high-risk areas or those with histol ogically free margins <1 mm. PMID:34630690 | PMC:PMC8495561 | DOI:10.3892/etm.2021.10771 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Panax notoginseng saponins alleviate osteoporosis and joint destruction in rabbits with antigen-induced arthritis

xlomafota13 shared this article with you from Inoreader <em>Panax notoginseng</em> saponins alleviate osteoporosis and joint destruction in rabbits with antigen-induced arthritis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1302. doi: 10.3892/etm.2021.10737. Epub 2021 Sep 16. ABSTRACT Although a number of anti-rheumatic drugs and biologics may be used to alleviate the symptoms of rheumatoid arthritis (RA), these compounds have been associated with bone loss and joint destruction; thus, alternative treatment approaches are required. In the present study, various plant extracts were evaluated for their capacity to inhibit joint destruction, and Panax notoginseng saponins (PNS), obtained from the Traditional Chinese Medicine Panax notoginseng, was identified as such a compound. Therefore, a rabbit antigen-induced arthritis (AIA) model was generated by immunization with ovalbumin in Freund's complete adjuvant, followed by treatment with PNS for 3 months. The morphology of the quadriceps femoris muscle, cartilage chondrocytes and skeletal elements was histologically observed by transmission electron microscopy (TEM), as well as micro-computed tomography. The results revealed that PNS significantly reduced the histopathological alterations associated with arthritic muscular atrophy and inflammation. In addition, TEM demonstrated that PNS protected chondrocytes from RA-associated damage. Furthermore, the bone density and microarchitecture in rabbits treated with PNS were markedly improved compared with those of the model group. Collectively, these data indicated that treatment with PNS may relieve osteoporosis and prevent joint and bone destruction in AIA. PMID:34630657 | PMC:PMC8461612 | DOI:10.3892/etm.2021.10737 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Blocking tumor necrosis factor-α delays progression of chronic obstructive pulmonary disease in rats through inhibiting MAPK signaling pathway and activating SOCS3/TRAF1

xlomafota13 shared this article with you from Inoreader Blocking tumor necrosis factor-α delays progression of chronic obstructive pulmonary disease in rats through inhibiting MAPK signaling pathway and activating SOCS3/TRAF1 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1311. doi: 10.3892/etm.2021.10746. Epub 2021 Sep 16. ABSTRACT The present study was conducted in order to study the detailed molecular mechanism of tumor necrosis factor (TNF)-α in chronic obstructive pulmonary disease (COPD). The rats were treated with cigarette smoke (CS) and lipopolysaccharide (LPS) to establish the COPD model. Next, the changes in lung injury in COPD rats with TNF-α knockdown was tested. Meanwhile, the regulation of TNF-α on MAPK pathway and its downstream molecules (SOCS3/TRAF1) was determined by western blotting. On this basis, the activation of MAPK and inhibition of SOCS3/TRAF1 was also examined. Subsequently, the lung function was tested with the plethysmograph, the cells of bronchoalveolar lavage fluid was counted and classified. Furthermore, lung tissue sections were stained with hematoxylin and eosin to verify whether the treatment of MAPK pathway and downstream molecules aff ected the effect of TNF-α knockdown on COPD. The present study showed that TNF-α knockdown could alleviate the decrease in the function and inflammatory injury of the lungs of rats with COPD. Western blot analysis verified that TNF-α knockdown could inhibit the activation of MAPK pathway and increase the expression of SOCS3/TRAF1. The following experimental results showed that the relief of lung injury caused by TNF-α knockdown could be deteriorated by activating MAPK pathway. It was also found that the symptom of COPD was decreased following transfection with sh-TNF-α but worsened by SOCS3/TRAF1 knockdown. Overall, TNF-α knockdown inhibited the activation of MAPK pathway and increased the expression of SOCS3/TRAF1, thus delaying the process of COPD. PMID:34630665 | PMC:PMC8461615 | DOI:10.3892/etm.2021.10746 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Enhanced expression of KIF4A in osteosarcoma predicts a poor prognosis and facilitates tumor growth by activation of the MAPK pathway

xlomafota13 shared this article with you from Inoreader Enhanced expression of KIF4A in osteosarcoma predicts a poor prognosis and facilitates tumor growth by activation of the MAPK pathway Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1339. doi: 10.3892/etm.2021.10774. Epub 2021 Sep 22. ABSTRACT The present study aimed to explore the prognostic value and role of kinesin family member 4A (KIF4A) expression in human osteosarcoma. KIF4A expression was evaluated in human osteosarcoma tissues from The Cancer Genome Atlas and Gene Expression Omnibus datasets. Reverse transcription-quantitative PCR was then applied to assess KIF4A level in both osteosarcoma cell lines and tissues. The association between KIF4A expression and clinical results in patients with osteosarcoma was detected by survival analysis. MTT assays and colony formation assays were used to evaluate the effects of KIF4A on osteosarcoma cell proliferation. The results indicated that the level of KIF4A was increased and associated with a poor prognosis in osteosarcoma tissues. Knockdown of KIF4A was shown to inhibit osteosarcoma cellular proliferation by affecting the MAPK pathway . The level of KIF4A was high in the human osteosarcoma tissues and this could be considered as a tumor induction gene, which may be used as an indicator of prognosis. PMID:34630693 | PMC:PMC8495555 | DOI:10.3892/etm.2021.10774 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

miR-638 suppresses proliferation by negatively regulating high mobility group A1 in ovarian cancer cells

xlomafota13 shared this article with you from Inoreader miR-638 suppresses proliferation by negatively regulating high mobility group A1 in ovarian cancer cells Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1319. doi: 10.3892/etm.2021.10754. Epub 2021 Sep 20. ABSTRACT Ovarian cancer is one of the most common gynecological diseases with high mortality rates. Previous studies have shown that microRNA (miR)-638 is associated with tumorigenesis. The present study aimed to assess the role and underlying mechanisms of miR-638 in ovarian cancer. miR-638 expression was detected in ovarian cancer tissues and miR-638 was overexpressed or knocked down in ovarian cancer OVCAR-3 and Caov-3 cells. The clinical results revealed that miR-638 expression was downregulated in ovarian cancer tissues compared with in adjacent normal tissues. miR-638 expression was also found to be relatively low in OVCAR-3 cells whilst being relatively high in Caov-3 cells among the five ovarian cancer cell lines tested. miR-638 overexpression inhibited cell viability, arrested the cell cycle at the G1 phase and promoted apoptosis in OV CAR-3 cells. By contrast, miR-638 knockdown increased Caov-3 cell viability, facilitated cell cycle progression and inhibited apoptosis. miR-638 reduced the expression of high mobility group A1 (HMGA1) by directly targeting its 3' untranslated region. HMGA1 overexpression reversed the inhibition of proliferation induced by miR-638 overexpression in OVCAR-3 cells. These results suggest that miR-638 may serve to be a suppressor of ovarian cancer by regulating HMGA1, which may provide a potential therapeutic target for ovarian cancer. PMID:34630673 | PMC:PMC8495545 | DOI:10.3892/etm.2021.10754 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Blood glucose control contributes to protein stability of Ski-related novel protein N in a rat model of diabetes

xlomafota13 shared this article with you from Inoreader Blood glucose control contributes to protein stability of Ski-related novel protein N in a rat model of diabetes Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1341. doi: 10.3892/etm.2021.10776. Epub 2021 Sep 22. ABSTRACT Ski-related novel protein N (SnoN) negatively regulates the transforming growth factor-β1 (TGF-β1)/Smads signaling pathway and is present at a low level during diabetic nephropathy (DN), but its underlying regulatory mechanism is currently unknown. The present study aimed to assess the effects of insulin-controlled blood glucose on renal SnoN expression and fibrosis in rats with diabetes mellitus (DM). Streptozotocin-induced DM rats were treated with insulin glargine (INS group) following successful model establishment. Blood samples were collected and centrifuged for biochemical indexes and the kidneys were collected for morphological analysis. In vitro, rat renal proximal tubular epithelial cells were treated with high-glucose medium for 24 h and transferred to normal glucose medium for 24 h. The expression levels of TGF-β1, SnoN, Sma d ubiquitin regulatory factor 2 (Smurf2), Arkadia, Smads, E-cadherin, α-smooth muscle actin and collagen III were assessed by western blotting and immunohistochemistry. The ubiquitylation of SnoN was detected by immunoprecipitation, and the expression levels of SnoN mRNA were evaluated by reverse transcription-quantitative PCR. The biochemical parameters and morphology indicated that renal fibrosis was notable in the DM group and mitigated in the INS group. Compared with the control group, TGF-β1, phosphor (p)-Smad2, p-Smad3, Smurf2 and Arkadia levels were enhanced in the DM group, and the levels of SnoN protein were decreased, whereas the levels of SnoN mRNA and ubiquitylation were increased in renal tissues. Notably, treatment with insulin reversed this trend. Furthermore, changing the glucose levels in the medium from high to normal glucose suppressed the epithelial-mesenchymal transition of NRK-52E cells by restoring the SnoN protein levels, and this phenomenon was impaired by the knockout of SnoN. SnoN protein levels were likely reduced through a mechanism enhanced by the ubiquitin proteasome system, which reversed the transcriptional activation of SnoN during DN progression. In addition, controlling blood glucose may delay DN fibrosis by rescuing the protein stability of SnoN. PMID:34630695 | PMC:PMC8495591 | DOI:10.3892/etm.2021.10776< /a> View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.