Browsing by Author "Nar, Rukiye"

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    Enhancement of Vascular Endothelial Growth Factor's Angiogenic Capacity by the Therapeutic Modulation of Notch Signalling Improves Tram Flap Survival in Rats Submitted to Nicotine
    (2017) Abbas, Ozan Luay; Terzi, Yunus Kasim; Ozatik, Orhan; Ozatik, Fikriye Yasemin; Turna, Gamze; Nar, Rukiye; Musmul, Ahmet; 0000-0001-5612-9696; 0000-0002-4662-6493; 0000-0002-8422-2975; 28277073; B-4372-2018; GXA-2381-2022; HOH-8201-2023
    Background: Smoke of cigarettes, and specifically nicotine, has been shown to diminish pedicled transverse rectus abdominis musculocutaneous (TRAM) flap survival. Considering that Notch signalling through its ligand Delta-like 4 (Dll4) functions as anti-angiogenic factor by inhibiting the pro-angiogenic effects of vascular endothelial growth factor (VEGF), it is hypothesised that inhibition of the Notch would promote angiogenesis and increase TRAM flap survival in rats submitted to nicotine. Methods: Twenty rats were treated with nicotine for 28 days preoperatively. Thereafter, a pedicled TRAM flap was created in all animals. The Notch inhibitor N-[N-(3,5-difluorophenacetyl)-1-alanyl]-S-phenylglycine-t-butyl-ester was administered in animals of the treatment group. Animals in the control group were given the same amount of solvent. Five days after the surgery, viable flap areas were determined. Skin samples were evaluated for VEGF and Dll4 mRNA levels. Immunohistochemical analysis was used for the assessment of endothelial Dll4 expression. Vascular density was determined histologically. Plasma levels of VEGF and Dll4 were measured. Results: A significant improvement in TRAM flap surviving area was observed in the treatment group (53.5014.25%) compared with the controls (32.20 +/- 9.15%). Immunohistochemical analysis revealed a significant increase in the number of Dll4 stained vessels in animals of the treatment group (9.2 +/- 1.6) in comparison with the controls (5.7 +/- 1.9). VEGF mRNA levels (0.22 +/- 0.08) in the treatment group were significantly lower than those in the control group (0.36 +/- 0.09). Conclusion: Notch inhibition significantly improved TRAM flap survival in animals exposed to nicotine by promoting VEGF-induced angiogenesis.
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    The Notch Signaling System Is Involved in the Regulation of Reparative Angiogenesis in the Zone of Stasis
    (2017) Abbas, Ozan Luay; Ozatik, Orhan; Terzi, Yunus Kasim; Ozatik, Fikriye Yasemin; Nar, Rukiye; Turna, Gamze; https://orcid.org/0000-0001-5612-9696; 28319529; B-4372-2018
    The Notch pathway ligand Delta-like 4 (Dll4) functions as an antiangiogenic factor, inhibiting vascular endothelial growth factor (VEGF)-induced angiogenesis. This function is documented in tumor and embryonic vasculature. However, its implication in burn wounds remains unexplored. Our objective was to explore the involvement of the Notch in the healing of zone of stasis burns. We hypothesized that anti-Dll4 therapy would prevent progressive necrosis in the stasis zone by promoting angiogenesis. Burns were created in 21 rats using the comb burn model. The Notch inhibitor N-[N-(3,5-difluorophenacetyl)1- alanyl]-S-phenylglycine-t-butyl-ester was administered in the treatment group. Controls were given the same amount of solvent. Seven days after the burn, skin samples were evaluated for VEGF and Dll4 gene expressions. Immunohistochemical analysis was used for the assessment of vascular density, endothelial Dll4 expression, and apoptosis count. Histologic grading of tissue damage was performed. Circulating levels of VEGF and Dll4 were determined. VEGF and Dll4 mRNA levels were found to be simultaneously induced after the burn. In the treatment group, a significant increase in the number of vessels was observed. However, gross evaluation documented an expansion of necrosis to the zone of stasis with marked activation of apoptosis. Histologic assessment showed that the resultant vascular overgrowth was accompanied by extensive edema and abundant infiltration of leukocytes. We provide evidence for the involvement of Notch in the regulation of angiogenesis in zone of stasis burns.