Tenascin and Fibronectin Expression after Pulp Capping with Different Hemostatic Agents: A Preliminary Study

This study investigated the expression of extracellular matrix glycoproteins tenascin (TN) and fibronectin (FN) in pulp repair after capping with calcium hydroxide (CH), following different hemostasis protocols. Class I cavities with a pulp exposure were prepared in 42 human third molars scheduled for extraction. Different hemostatic agents (0.9% saline solution, 5.25% sodium hypochlorite and 2% chlorhexidine digluconate) were used and pulps were capped with CH cement. After 7, 30 or 90 days, teeth were extracted, formalin-fixed, and prepared for immunohistochemical technique. Hemostatic agents did not influence the expression of TN and FN. Both glycoproteins were found in the entire the pulp tissue and around collagen fibers, but were absent in the mineralized tissues. In the predentin, TN showed positive immunostaining and FN had a variable expression. Within 7 days post-treatment, a slightly more pronounced immunostaining on the pulp exposure site was observed. Within 30 days, TN and FN demonstrated a positive expression around the dentin barrier and at 90 days, a thin and linear expression of TN and FN was delimitating the reparative dentin. In conclusion, hemostatic agents did not influence TN and FN expression. Immunostaining for TN and FN was seen in different regions and periods, demonstrating their role in pulp repair.

Este estudo investigou a expressão das glicoproteínas Tenascina (TN) e Fibronectina (FN) da matriz extracelular no reparo pulpar após capeamento com hidróxido de cálcio (HC), seguindo diferentes protocolos de hemostasia. Cavidades de classe I com exposição pulpar foram preparadas em 42 terceiros molares humanos indicados para extração. Diferentes agentes hemostáticos (solução salina a 0,9%, hipoclorito de sódio a 5,25% e clorexidina a 2%) foram usados e as polpas foram capeadas com cimento de HC. Após 7, 30 ou 90 dias, os dentes foram extraídos, fixados em formalina e preparados para análise imunoistoquímica. Os agentes hemostáticos não influenciaram a expressão de TN e FN. Ambas glicoproteínas foram encontradas em todo tecido pulpar, ao redor das fibras colágenas e estiveram ausentes nos tecidos mineralizados. Na pré-dentina, a TN mostrou forte imunoexpressão e a FN teve uma expressão variável. Após 7 dias, foi observada uma expressão levemente mais pronunciada no lugar da exposição pulpar. Aos 30 dias, a TN e a FN demonstraram uma expressão mais forte sob a barreira dentinária e aos 90 dias, uma expressão fina e linear da TN e FN apresentava-se delimitando a dentina reparativa. Em conclusão, os agentes hemostáticos não influenciaram e expressão da TN e da FN. A imunoexpressão da TN e FN foi observada em diferentes regiões e períodos, demonstrando o seu papel no reparo pulpar.

Imatinib atenua a fibrose miocárdica em associação com a inibição da atividade do PDGFRα / Imatinib attenuates myocardial fibrosis in association with inhibition of the PDGFRα activity

FUNDAMENTO: O Imatinib é um inibidor do receptor tirosina-quinase que foi confirmada como exercendo um efeito inibidor sobre a atividade do receptor do PDGF, fator de crescimento plaquetário (PDGFRα e PDGFRβ). OBJETIVO: Investigar o efeito protetor do Imatinib na fibrose miocárdica em acetato de deoxicorticosterona (DOCA)/ratos com hipertensão induzida por sal. MÉTODOS: Sessenta ratos Sprague-Dawley machos, uninefrectomizados foram distribuídos em três grupos: ratos controles (grupo CON): grupo deoxicorticosterona (grupo DOCA); grupo deoxicorticosterona e Imatinib (grupo DOCA IMA). A Pressão Arterial Sistólica (PAS) foi medida quinzenalmente. Foi estudada a porção apical do ventrículo esquerdo. Foram empregados: coloração vermelho sirius, coloração de hematoxilina-eosina, imuno-histoquímica e ensaio de western blot. RESULTADOS: A PAS nos grupos DOCA e IMA+DOCA foi maior que no grupo CON nos dias 14 e 28. Os animais do grupo DOCA apresentaram fibrose intersticial e perivascular grave no dia 28, e as expressões de PI, PIII, tenascina-C e fibronectina foram significativamente maiores que nos grupos DOCA+IMA e CON. Quando comparados com o grupo CON, os grupos DOCA e DOCA+IMA apresentaram resposta inflamatória de tecido miocárdico e infiltração de monócitos/macrófagos de diferentes graus. As expressões proteicas do PDGF-A, PDGF-C e PDGFRα foram significativamente maiores nos grupos DOCA e DOCA+IMA que no grupo CON, mas a expressão proteica do p-PDGFRα no grupo DOCA+IMA foi menor que no DOCA. CONCLUSÃO: O Imatinib pode exercer efeitos inibitórios sobre a fibrose miocárdica em ratos com hipertensão induzida por DOCA/sal, os quais podem ser atribuídos à inibição da atividade do PDGFR-α.

BACKGROUND: Imatinib is a tyrosine kinase receptor inhibitor that has been confirmed to exert inhibitory effect on the platelet derived growth factor PDGF receptor (PDGFRα and PDGFRβ) activity. OBJECTIVE: To investigate the protective effect of imatinib on the myocardial fibrosis in deoxycorticosterone-acetate (DOCA)/salt induced hypertensive rats. METHODS: Sixty male uninephrectomized Sprague-Dawley rats were assigned to three groups: control rats (CON group); deoxycorticosterone group (DOCA group); deoxycorticosterone and imatinib group (DOCA+IMA group). Systolic blood pressure (SBP) was measured biweekly. The apical portion of the left ventricle was studied. Sirius-Red staining, Hematoxylin-Eosin staining, immunohistochemistry and Western blot assay were employed. RESULTS: SBP in the DOCA group and DOCA+IMA group was higher than that in the CON group on day 14 and 28. Animals in the DOCA group showed severe interstitial and perivascular fibrosis on day 28, and the expressions of PI, PIII, tenascin-C and fibronectin were significantly higher than those in the DOCA+IMA group and CON group. When compared with the CON group, myocardial tissue inflammatory response and monocyte/macrophage infiltration of different degrees were observed in the DOCA group and DOCA+IMA group. Protein expressions of PDGF-A, PDGF-C and PDGFRα were signiflcantly higher in the DOCA and DOCA+IMA groups than those in the CON group, but the p-PDGFRα protein expression in the DOCA+IMA group was lower than that in the DOCA group. CONCLUSION: Imatinib can exert inhibitory effects on myocardial fibrosis in DOCA/salt induced hypertensive rats, which may be attributed to the inhibition of PDGFR-α activity.

Biochemical evaluation of the supporting structure of pelvic organs in selected numbers of premenopausal and postmenopausal Malaysian women.

Context: Pelvic organ prolapse (POP) is associated with menopause and changes in the proteins of the pelvic supporting system, but there is scant data on the precise alterations in Malaysian women. Aim: The aim of this study is to determine the differences in the extracellular matrices (ECM) of uterosacral ligaments in premenopausal and postmenopausal Malaysian women with or without POP. Settings and Design: The observational study was conducted for 9 months in three general hospitals involving 30 women who underwent hysterectomies for various indications except for carcinoma of pelvic organs. Materials and Methods: Three groups were identified: Premenopausal women (Group 1), postmenopausal women without POP (Group 2), and postmenopausal women with POP (Group 3). Age, duration of menopause, body mass index (BMI), parity, and vaginal deliveries were documented. Only 21 samples of the uterosacral ligaments were stained immunohistochemically for collagen I and III, matrix metalloproteinases (MMPs) 1 and 2, elastin, and tenascin. Statistical Analysis Used: Image J software analysis was utilized for quantification, while non-parametric statistics (Kruskal-Wallis with post-hoc Dunns Multiple Comparison test) was used for result analysis. Results: The profile parameters were not significantly different except for mean age and duration of menopause in Group 3. Samples from Group 2 showed lower expression of almost all proteins except MMP1 and tenascin (higher) as compared to Group 1. The changes appeared to be exaggerated in Group 3, though statistically insignificant. Conclusion: A significant difference in the expression of ECM was apparent in postmenopausal subjects as compared to premenopausal ( P = 0.05), compromising the uterosacral ligament tensile strength. The findings are proven similar as those changes in women from other studies.

Caracterização imuno-histoquímica de lesão híbrida de ameloblastoma desmoplásico e convencional / Hybrid lesion of desmoplastic and conventional ameloblastoma: immunohistochemical aspects

O ameloblastoma é uma neoplasia odontogênica benigna comumente encontrada nos ossos maxilares. Histologicamente, mostra diversos padrões, incluindo a ameloblastoma plexiforme e folicular. Quando estes padrões histológicos coexistem com um ameloblastoma que exibe abundante desmoplasia, são então denominados de lesão æhíbrida" de ameloblastoma desmoplásico e convencional. No presente trabalho, nos propomos a relatar um caso de lesão híbrida de ameloblastoma desmoplásico e convencional destacando os aspectos imuno-histoquímicos relativos a expressão das proteínas da matriz extracelular (tenascina, fibronectina e colágeno I).

Ameloblastoma is a benign epithelial odontogenic tumor and is the most commonly encountered odontogenic tumor in the jaws. Histologically, ameloblastomas occur in different patterns, including plexiform pattern and follicular pattern. "Hybrid " lesion of ameloblastoma is a tumor variant in which histologically, areas of follicular or plexiform ameloblastoma coexist with characteristic areas of ameloblastoma exhibiting pronounced stromal desmoplasia (desmoplastic ameloblastoma). The purpose of this article is to present a case of "hybrid" lesion of desmoplastic ameloblastoma (AD) and conventional, and investigate extracellular matrix proteins such as tenascin, fibronectin, and type I collagen.

Ongoing angiogenesis in blood vessels of the abdominal aortic aneurysm

Pathogenesis of the abdominal aortic aneurysm has been attributed to neovascularization of the aortic wall. However, it is not clear whether angiogenesis persists in the aneurysm. In sections of aneurysms, we determined the immunohistochemical distributions of the alpha v beta 3 integrin, tenascin and endothelial nitric oxide synthase (eNOS), which are markers respectively, of angiogenesis, matrix remodeling and vasoregulatory function. In addition, we used reverse transcription followed by in situ PCR, to determine the distribution of alpha v mRNA. All aneurysm specimens exhibited extensive increases of wall vascularization as compared with the control aortic wall, and showed the presence of perivascular inflammatory exudates containing macrophages and lymphocytes. The neovascularization consisted of thick-walled vessels in the media and adventitia, and capillaries in the subintima. The majority of vessels stained positively for the alpha v beta 3 antigen and eNOS. Tenascin was deposited as bands that circumscribed thick-walled vessels. The distribution of av mRNA was extensive and was positive even in those vessels that failed to stain for the alpha v beta 3 protein. No staining was evident in control aortas for the alpha v beta 3 antigen, tenascin or alpha v mRNA. The upregulation of av mRNA and the alpha v beta 3 integrin in blood vessels surrounded by a matrix expressing tenascin, indicates that angiogenesis is an ongoing process in the mature aortic aneurysm.