Researcher:
Göktaş, Selda

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Selda

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Göktaş

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Göktaş, Selda

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2015 - 20203

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    Hemodynamic flow visualization of early embryonic great vessels using μPIV
    (Humana Press Inc, 2015) Chen, Chia-Yuan; Kowalski, William J.; Pekkan, Kerem; N/A; Göktaş, Selda; Researcher; N/A; N/A
    Microparticle image velocimetry (mu PIV) is an evolving quantitative methodology to closely and accurately monitor the cardiac flow dynamics and mechanotransduction during vascular morphogenesis. While PIV technique has a long history, contemporary developments in advanced microscopy have significantly expanded its power. This chapter includes three new methods for mu PIV acquisition in selected embryonic structures achieved through advanced optical imaging: (1) high-speed confocal scanning of transgenic zebrafish embryos, where the transgenic erythrocytes act as the tracing particles; (2) microinjection of artificial seeding particles in chick embryos visualized with stereomicroscopy; and (3) real-time, timeresolved optical coherence tomography acquisition of vitelline vessel flow profiles in chick embryos, tracking the erythrocytes.
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    Microstructure of early embryonic aortic arch and its reversibility following mechanically altered hemodynamic load release
    (Amer Physiological Soc, 2020) Department of Mechanical Engineering; N/A; N/A; N/A; N/A; Department of Mechanical Engineering; Department of Mechanical Engineering; Department of Mechanical Engineering; Çelik, Merve; Göktaş, Selda; Karakaya, Cansu; Çakıroğlu, Ayşe İdil; Karahüseyinoğlu, Serçin; Lashkarinia, Seyedeh Samaneh; Ermek, Erhan; Pekkan, Kerem; Undergraduate Student; Resercher; Master Student; Researcher; Faculty Member; Researcher; Other; Faculty Member; Department of Mechanical Engineering; College of Sciences; N/A; Graduate School of Sciences and Engineering; N/A; School of Medicine; College of Engineering; College of Engineering; College of Engineering; N/A; N/A; N/A; N/A; 110772; N/A; N/A; 161845
    In the embryonic heart, blood flow is distributed through a bilaterally paired artery system composed of the aortic arches (AAs). The purpose of this study is to establish an understanding of the governing mechanism of microstructural maturation of the AA matrix and its reversibility, toward the desired macroscopic vessel lumen diameter and thickness for healthy, abnormal, and in ovo repaired abnormal mechanical loading. While matrix-remodeling mechanisms were significantly different for normal versus conotruncal banding (CTB), both led to an increase in vessel lumen. Correlated with right-sided flow increase at Hamburger & Hamilton stages 21, intermittent load switching between collagen I and III with elastin and collagen-IV defines the normal process. However, decreases in collagen I. elastin, vascular endothelial growth factor-A, and fibrillin-1 in CTB were recovered almost fully following the CTB-release model, primarily because of the pressure load changes. The complex temporal changes in matrix proteins are illustrated through a predictive finite-element model based on elastin and collagen load-sharing mechanism to achieve lumen area increase and thickness increase resulting from wall shear stress and tissue strain, respectively. The effect of embryonic timing in cardiac interventions on AA microstructure was established where abnormal mechanical loading was selectively restored at the key stage of development. Recovery of the normal mechanical loading via early fetal intervention resulted in delayed microstructural maturation. Temporal elastin increase, correlated with wall shear stress, is required for continuous lumen area growth. NEW & NOTEWORTHY The present study undertakes comparative analyses of the mechanistic differences of the arterial matrix microstructure and dynamics in the three fundamental processes of control, conotruncal banded, and released conotruncal band in avian embryo. Among other findings, this study provides specific evidence on the restorative role of elastin during the early lumen growth process. During vascular development. a novel intermittent load-switching mechanism between elastin and collagen, triggered by a step increase in wall shear stress, governs the chronic vessel lumen cross-sectional area increase. Mimicking the fetal cardiovascular interventions currently performed in humans, the early release of the abnormal mechanical load rescues the arterial microstructure with time lag.
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    Asymmetry in mechanosensitive gene expression during aortic arch morphogenesis
    (Nature Publishing Group (NPG), 2018) Kowalski, William J.; Keller, Bradley B.; Department of Mechanical Engineering; Pekkan, Kerem; Karakaya, Cansu; Göktaş, Selda; Çelik, Merve; Faculty Member; Master Student; Researcher; Undergraduate Student; Department of Mechanical Engineering; Graduate School of Sciences and Engineering; 161845; N/A; N/A; N/A
    Embryonic aortic arches (AA) are initially bilaterally paired, transitional vessels and failures in remodeling based on hemodynamic and growth-related adaptations cause a spectrum of congenital heart disease (CHD) anatomies. Identifying regulatory mechanisms and cross-talk between the genetic elements of these vessels are critical to understand the ethiology of CHD and refine predictive computational models. This study aims to screen expression profiles of fundamental biological pathways in AA at early stages of chick embryo morphogenesis and correlate them with our current understanding of growth and mechanical loading. Reverse transcription-quantitative PCR (RT-qPCR) was followed by correlation and novel peak expression analyses to compare the behaviour and activation period of the genes. Available protein networks were also integrated to investigate the interactions between molecules and highlight major hierarchies. Only wall shear stress (WSS) and growth-correlated expression patterns were investigated. Effect of WSS was seen directly on angiogenesis as well on structural and apoptosis-related genes. Our time-resolved network suggested that WSS-correlated genes coordinate the activity of critical growth factors. Moreover, differential gene expression of left and right AA might be an indicator of subsequent asymmetric morphogenesis. These findings may further our understanding of the complex processes of cardiac morphogenesis and errors resulting in CHD.