Visitsattapongse, Sarinporn

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Visitsattapongse, Sarinporn
Alternative Name
Visitsattapongse, S.
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Email
sarinporn.vi@kmitl.ac.th

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    Store-operated calcium entry facilitates LPS-induced superoxide anion-dependent macrophage extracellular traps
    (2025-07-09)
    Nguyen, Thang Ngoc
    ;
    Lin, Tzu Chien
    ;
    Chimphlee, Waratchaya
    ;
    Siew, Kon Xuen
    ;
    Vongmanee, Naphatsawan
    Macrophage extracellular traps (METs) represent a recently discovered complex defence mechanism that is distinct from phagocytosis and involves the release of DNA and antibacterial proteins. They play an important role in pathogen removal, and calcium ions (Ca 2+) have also been reported to be involved. In the present study, we identified METotic cells using digitonin as an alternative to Triton X-100, coupled with immunofluorescence staining using lamin antibodies. The limited permeability of digitonin ensures exclusive intranuclear antibody labelling of MET cells, therefore providing a straightforward and intuitive differentiation method. We found that under lipopolysaccharide stimulation, macrophages undergo store-operated Ca 2+ entry (SOCE) to facilitate Ca 2+ influx. Elevation of cytoplasmic Ca 2+ levels by SOCE promotes the generation of superoxide anions by NADPH oxidase (NOX), ultimately leading to METosis. In summary, our study strengthens the role of Ca 2+ in NOX-dependent METosis, which differs from previous studies focusing on Ca 2+ in the NOX-independent pathway. Our research reveals that Ca 2+ -mediated regulation of NOX plays a crucial role in METosis, especially in SOCE, and provides novel ideas for future research.
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    Electrochemical Biosensors by Means of Molecularly Imprinted Polymers (MIPs) Cortisol Recognition
    (2025-02-01)
    Nampeng, Jindapa
    ;
    Vongmanee, Naphatsawan
    ;
    Pintavirooj, Chuchart
    ;
    Chiu, Wen Tai
    ;
    Visitsattapongse, Sarinporn
    Depression and anxiety are two common mental health issues that require serious attention, as they have significant impacts on human well-being, with both being emotionally and physically reflected in the increasing number of suicide cases globally. The World Health Organization (WHO) estimated that about 322 million people around the world experienced mental illnesses in 2017, and this number continues to increase. Cortisol is a major stress-controlled hormone that is regulated by the hypothalamic–pituitary–adrenal (HPA) axis. The HPA axis has three main components, including the hypothalamus, pituitary gland, and adrenal gland, where cortisol, the primary stress hormone, is released. It plays crucial roles in responding to stress, energy balance, and the immune system. The cortisol level in the bloodstream usually increases when stress develops. Molecularly imprinted polymers (MIPs) have been highlighted in terms of creating artificial bioreceptors by mimicking the shape of detected biomolecules, making natural bioreceptor molecules no longer required. MIPs can overcome the limitations of chemicals and physical properties reducing over time and the short-time shelf life of natural bioreceptors. MIPs’ benefits are reflected in their ease of use, high sensitivity, high specificity, reusability, durability, and the lack of requirement for complicated sample preparation before use. Moreover, MIPs incur low costs in manufacturing, giving them a favorable budget for the market with simple utilization. MIPs can be formulated by only three key steps, including formation, the polymerization of functional monomers, and the creation of three-dimensional cavities mimicking the shape and size of targeting molecules. MIPs have a high potential as biosensors, especially working as bioanalytics for protein, anti-body, antigen, or bacteria detection. Herein, this research proposes an MIP-based cortisol biosensor in which cortisol is imprinted on methyl methacrylate (MMA) and methacrylic acid (MAA) produced by UV polymerization. This MIP-based biosensor may be an alternative method with which to detect and monitor the levels of hormones in biological samples such as serum, saliva, or urine due to its rapid detection ability, which would be of benefit for diagnosing depression and anxiety and prescribing treatment. In this study, quantitative detection was performed using an electrochemical technique to measure the changes in electrical signals in different concentrations of a cortisol solution ranging from 0.1 to 1000 pg/mL. The MIP-based biosensor, as derived by calculation, achieved its best detection limit of 1.035 pg/mL with a gold electrode. Tests were also performed on molecules with a similar molecular structure, including Medroxyprogesterone acetate and drospirenone, to ensure the sensitivity and accuracy of the sensors, demonstrating a low sensitivity and low linear response.
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    YAP inactivation-mediated autophagy inhibition contributes to cisplatin resistance in ovarian cancer cells
    (2026-12-01)
    Nguyen, Ngoc Thang
    ;
    Hsieh, Meng Ru
    ;
    Nguyen, Hieu Dac Hanh
    ;
    Chimphlee, Waratchaya
    ;
    Visitsattapongse, Sarinporn
    Background: Cisplatin resistance remains a critical barrier in the treatment of high-grade serous ovarian cancer (HGSOC). Although Hippo−YAP signaling regulates cancer progression, its contribution to cisplatin resistance is still poorly understood. Here, we demonstrate that YAP is inactivated and sequestered in the cytoplasm of cisplatin-resistant ovarian cancer cells. Results: This cytosolic retention is mediated by Hippo kinases MST1/2 and LATS1/2, as well as ERK signaling, resulting in increased phosphorylation of YAP at its inhibitory site (Ser397) and reduced phosphorylation at its activating site (Tyr357). Restoration of YAP activity through genetic overexpression or pharmacological induction of nuclear YAP accumulation significantly reversed cisplatin resistance. Mechanistically, YAP inactivation impaired cisplatin-induced autophagy. Cisplatin robustly triggered autophagy in parental cells, as evidenced by LC3 puncta formation; however, this autophagic response was blunted in resistant cells. Overexpression of YAP further suppressed LC3 puncta formation and Beclin-1 expression, and increased p62 accumulation in cisplatin-resistant ovarian cancer cells. Autophagy inhibition using 3-methyladenine (3-MA) resensitized resistant cells to cisplatin. Conclusion: Collectively, these findings reveal that YAP inactivation contributes to cisplatin resistance by abrogating autophagy formation and identify YAP reactivation as a potential strategy to overcome chemoresistance in ovarian cancer.
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    Bcl-2 upregulates calcium efflux through PMCA and NCX1 to preserve intracellular calcium homeostasis and confer resistance to apoptosis
    (2026-07-01)
    Lin, Tzu Chien
    ;
    Lee, Ming Jyun
    ;
    Nguyen, Ngoc Thang
    ;
    Hsiao, Shih Chuan
    ;
    Chen, Ying Chi
    Bcl-2 has been shown to regulate intracellular calcium (Ca²⁺) homeostasis, thereby influencing cellular metabolism, survival, and apoptosis. While previous studies have primarily focused on Bcl-2′s role in modulating Ca²⁺ levels within the endoplasmic reticulum and mitochondria, extracellular Ca²⁺ is a major determinant of cellular activation and Ca²⁺ homeostasis. Therefore, it is important to investigate whether Bcl-2 also contributes to the regulation of Ca²⁺ flux across the plasma membrane. A vector control, wild-type Bcl-2, and a Bcl-2 mutant were stably expressed in MDCK (Madin-Darby Canine Kidney) cells that lacked endogenous Bcl-2 expression. Real-time intracellular Ca²⁺ measurements by a single-cell fluorimeter were performed to measure Ca²⁺ release and influx with the ratiometric Ca<sup>2+</sup> indicator Fura-2 AM. Our results demonstrate that Bcl-2 enhances store-operated Ca²⁺ entry (SOCE)-mediated Ca²⁺ influx, a key mechanism underlying spontaneous Ca²⁺ oscillations. Furthermore, Bcl-2 upregulates the expression of plasma membrane Ca²⁺ ATPase (PMCA) and Na<sup>+</sup>-Ca²⁺ exchanger 1 (NCX1), which mediate Ca²⁺ extrusion from the cytosol. Pharmacological inhibition of PMCA with resveratrol (RES) and of NCX1 with ORM-10103 suppressed spontaneous Ca²⁺ oscillations, with PMCA playing a more dominant role than NCX1. Additionally, both RES and ORM-10103 exacerbated thapsigargin-induced Ca²⁺ cytotoxicity. Collectively, our findings reveal that Bcl-2 promotes Ca²⁺ influx to sustain oscillatory signaling and facilitates Ca²⁺ efflux to prevent cytotoxic accumulation, thereby maintaining Ca²⁺ homeostasis. This dual regulatory function provides new insights into Bcl-2–mediated Ca²⁺ signaling and its biological significance in apoptosis inhibition, independent of its interactions with other Bcl-2 family proteins.