Browsing by Subject "PlGF"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    Open Access
    Placental growth factor and soluble Fms-like tyrosine kinase 1 in diabetic pregnancy: A possible relation to distal villous immaturity
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) El-Tarhouny, Shereen A.; Almasry, Shaima M.; Elfayomy, Amr K.; Baghdadi, Hussam; Habib, Fawzia A.
    This study aimed to describe the prevalence of chorionic distal villous immaturity (DVI) in overt diabetic/gestational diabetic (OD/GD) women compared with normoglycemic ones and to analyze the relation of DVI index (DVII) to placental growth factor (PlGF) and soluble Fms-like tyrosine kinase 1 (sFlt-1). Three groups were studied; normoglycemics (n=21), OD (n=17) and GD (n=20). Maternal blood samples were evaluated regarding serum levels of PlGF and sFlt-1. Immunohistochemical methodologies were employed in term placentae of all subjects to assess DVII and area% of PlGF and sFlt-1 immunostaining. We found that mean Hemoglobin A1c (HbA1c) is 5.22±0.15 in normoglycemics, 6.2±0.3 in OD, and 5.70±0.23 in GD with significant differences between groups (p=0.012). DVII was significantly higher in OD (66.6±4.7) and GD (72.4±4.5) compared to controls (11.6±2.5; p=0.000). Healthy women have significantly lower levels of PlGF (86.6±14.5) compared to OD (166.6±22.4, p=0.000) and GD (150.3±23.97, p=0.000) and their placentae expressed a significantly lower area% of PlGF (6.5±0.8) compared to OD (14.8±1.0, p=0.000) and GD (18.8±1.3, p=0.000). Also, normoglycemic women have significantly lower levels of sFlt-1 (108.9±12.1) compared to OD (226.5±18.6, p=0.000) or GD (197.2±16.8, p=0.000) and their placentae expressed a significantly lower area% of sFlt-1 (3.2±0.3) compared to OD (15.4±1.7, p=0.000) and GD (16.9±1.2, p=0.000). There was significant correlation between DVII and both serum level and area% of PlGF and sFlt-1 expression in the 3 groups. This study provided a new score for evaluating DVI in normal and diabetic placentae and suggested a role for PlGF and sFlt-1 in regulation of DVI in diabetic pregnancies.
  • Thumbnail Image
    Publication
    Open Access
    PlGF/Flt-1/MMP-1 axis in gingival carcinoma bone invasion
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Nguyen Phuong Thao; Miyauchi Mutsumi; Subarnbhesaj Ajiravudh; Ogawa Ikuko; Chea Chanbora; Takata Takashi; Biología Celular e Histología
    Background. Gingival squamous cell carcinoma (SCC) frequently invades adjacent bone tissue, leading to significant morbidity and mortality. Understanding the molecular mechanisms driving bone invasion is crucial for developing targeted therapies. We investigated the role of placental growth factor (PlGF) in this process, focusing on its interaction with RANKL and MMP-1. Methods. We examined the role of PlGF in bone invasion of gingival SCC through analysis of patient samples (n=55) and various in-vitro assays, including an in-vitro bone-cell coculture system. We investigated the molecular mechanisms underlying PlGF-mediated bone invasion and its relationship with RANKL and MMP-1 expression. Results. Our findings demonstrate that gingival SCC-secreted PlGF promotes local bone invasion through two possible ways: 1) direct induction of RANKL expression, activating osteoclast formation and bone resorption, and 2) indirect upregulation of RANKL via MMP-1 signaling. PlGF secretion by tumor cells triggered RANKL and MMP-1 production and significantly stimulated migration and osteoclastogenesis (p<0.05). Furthermore, PlGF is highly expressed in gingival SCC and significantly correlated with bone invasion. Finally, we also confirmed the significantly positive correlation between expression levels of MMP-1 with PlGF and Flt-1 expression. Conclusion. This study identifies PlGF as a key regulator of osteoclastogenesis in gingival SCC through both direct and MMP-1-mediated pathways. Therefore, targeting PlGF activity may represent a potential therapeutic strategy for inhibiting bone invasion in gingival SCC