Publications by authors named "H Kitasato"
Article Synopsis
- Patients with COVID-19 often suffer from acute kidney injury, linked to disease severity, which involves loss of a protein called megalin in kidney cells that affects vitamin D metabolism.
- A study using mice infected with SARS-CoV-2 showed reduced levels of megalin, indicating kidney damage, along with changes in vitamin D-related gene expression.
- Despite similar serum vitamin D levels between infected and non-infected mice, the loss of megalin may alter how vitamin D affects immune responses in the kidneys during infection.
Introduction: Cardiac remodeling is defined as cellular interstitial changes that lead dysfunction of the heart after injury. Placental growth factor (PlGF), a member of the VEGF family, has been reported to regulate cardiac hypertrophy in hemodynamic state. We therefore analyze the function of PlGF during cardiac remodeling using cardiac cells and fibroblasts, under Angiotensin II (AngII) stimulation.
View Article and Find Full Text PDFCoronavirus disease 2019 (COVID-19) is an infectious viral disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that emerged at the end of 2019. SARS-CoV-2 can be transmitted through droplets, aerosols, and fomites. Disinfectants such as alcohol, quaternary ammonium salts, and chlorine-releasing agents, including hypochlorous acid, are used to prevent the spread of SARS-CoV-2 infection.
View Article and Find Full Text PDFAims: Microsomal prostaglandin E synthase-1 (mPGES-1)/prostaglandin E2 (PGE2) induces angiogenesis through the prostaglandin E2 receptor (EP1-4). Among immune cells, regulatory T cells (Tregs), which inhibit immune responses, have been implicated in angiogenesis, and PGE2 is known to modulate the function and differentiation of Tregs. We hypothesized that mPGES-1/PGE2-EP signalling could contribute to recovery from ischaemic conditions by promoting the accumulation of Tregs.
View Article and Find Full Text PDFBackground: Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme that acts downstream of cyclooxygenase and plays a major role in inflammation by converting prostaglandin (PG) H to PGE. The present study investigated the effect of genetic deletion of mPGES-1 on the development of immunologic responses to experimental colitis induced by dextran sodium sulfate (DSS), a well-established model of inflammatory bowel disease (IBD).
Methods: Colitis was induced in mice lacking mPGES-1 (mPGES-1 mice) and wild-type (WT) mice by administering DSS for 7 days.