LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 3 of total 3

Search options

  1. Article ; Online: Corrigendum to Zhang J, Cai J, Cui Y, Jiang S, Wei J, Kim YC, Chan J, Thalakola A, Le T, Xu L, Wang L, Jiang K, Wang X, Wang H, Cheng F, Buggs J, Koepsell H, Vallon V, Liu R. "Role of the macula densa sodium glucose cotransporter type 1-neuronal nitric oxide synthase-tubuloglomerular feedback pathway in diabetic hyperfiltration." Kidney Int. 2022;101:541-550.

    Zhang, Jie / Cai, Jing / Cui, Yu / Jiang, Shan / Wei, Jin / Kim, Young Chul / Chan, Jenna / Thalakola, Anish / Le, Thanh / Xu, Lan / Wang, Lei / Jiang, Kun / Wang, Ximing / Wang, Haibo / Cheng, Feng / Buggs, Jacentha / Koepsell, Hermann / Vallon, Volker / Liu, Ruisheng

    Kidney international

    2022  Volume 102, Issue 2, Page(s) 448

    Language English
    Publishing date 2022-07-20
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2022.05.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Role of the macula densa sodium glucose cotransporter type 1-neuronal nitric oxide synthase-tubuloglomerular feedback pathway in diabetic hyperfiltration.

    Zhang, Jie / Cai, Jing / Cui, Yu / Jiang, Shan / Wei, Jin / Kim, Young Chul / Chan, Jenna / Thalakola, Anish / Le, Thanh / Xu, Lan / Wang, Lei / Jiang, Kun / Wang, Ximing / Wang, Haibo / Cheng, Feng / Buggs, Jacentha / Koepsell, Hermann / Vallon, Volker / Liu, Ruisheng

    Kidney international

    2021  Volume 101, Issue 3, Page(s) 541–550

    Abstract: An increase of glomerular filtration rate (GFR) is a common observation in early diabetes and is considered a key risk factor for subsequent kidney injury. However, the mechanisms underlying diabetic hyperfiltration have not been fully clarified. Here, ... ...

    Abstract An increase of glomerular filtration rate (GFR) is a common observation in early diabetes and is considered a key risk factor for subsequent kidney injury. However, the mechanisms underlying diabetic hyperfiltration have not been fully clarified. Here, we tested the hypothesis that macula densa neuronal nitric oxide synthase (NOS1) is upregulated via sodium glucose cotransporter type 1 (SGLT1) in diabetes, which then inhibits tubuloglomerular feedback (TGF) promoting glomerular hyperfiltration. Therefore, we examined changes in cortical NOS1 expression and phosphorylation, nitric oxide production in the macula densa, TGF response, and GFR during the early stage of insulin-deficient (Akita) diabetes in wild-type and macula densa-specific NOS1 knockout mice. A set of sophisticated techniques including microperfusion of juxtaglomerular apparatus in vitro, micropuncture of kidney tubules in vivo, and clearance kinetics of plasma fluorescent-sinistrin were employed. Complementary studies tested the role of SGLT1 in SGLT1 knockout mice and explored NOS1 expression and phosphorylation in kidney biopsies of cadaveric donors. Diabetic mice had upregulated macula densa NOS1, inhibited TGF and elevated GFR. Macula densa-selective NOS1 knockout attenuated the diabetes-induced TGF inhibition and GFR elevation. Additionally, deletion of SGLT1 prevented the upregulation of macula densa NOS1 and attenuated inhibition of TGF in diabetic mice. Furthermore, the expression and phosphorylation levels of NOS1 were increased in cadaveric kidneys of diabetics and positively correlated with blood glucose as well as estimated GFR in the donors. Thus, our findings demonstrate that the macula densa SGLT1-NOS1-TGF pathway plays a crucial role in the control of GFR in diabetes.
    MeSH term(s) Animals ; Diabetes Mellitus, Experimental/metabolism ; Feedback ; Glomerular Filtration Rate/physiology ; Kidney Glomerulus/metabolism ; Kidney Tubules/metabolism ; Mice ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type I/genetics ; Nitric Oxide Synthase Type I/metabolism ; Sodium-Glucose Transporter 1/metabolism
    Chemical Substances Slc5a1 protein, mouse ; Sodium-Glucose Transporter 1 ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type I (EC 1.14.13.39)
    Language English
    Publishing date 2021-11-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2021.10.037
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: Knockout of Macula Densa Neuronal Nitric Oxide Synthase Increases Blood Pressure in db/db Mice.

    Zhang, Jie / Wang, Ximing / Cui, Yu / Jiang, Shan / Wei, Jin / Chan, Jenna / Thalakola, Anish / Le, Thanh / Xu, Lan / Zhao, Liang / Wang, Lei / Jiang, Kun / Cheng, Feng / Patel, Trushar / Buggs, Jacentha / Vallon, Volker / Liu, Ruisheng

    Hypertension (Dallas, Tex. : 1979)

    2021  Volume 78, Issue 6, Page(s) 1760–1770

    Abstract: Figure: see text]. ...

    Abstract [Figure: see text].
    MeSH term(s) Animals ; Blood Pressure/genetics ; Glomerular Filtration Rate/genetics ; Hemodynamics/genetics ; Kidney Glomerulus/metabolism ; Mice ; Mice, Knockout ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type I/genetics
    Chemical Substances Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type I (EC 1.14.13.39)
    Language English
    Publishing date 2021-10-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.121.17643
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top