Depressed expression of Klotho and FGF receptor 1 in hyperplastic parathyroid glands from uremic patients | Zendy

Hirotaka Komaba | Zendy; Shunsuke Goto | Zendy; Hideki Fujii | Zendy; Yasuhiro Hamada | Zendy; Akira Kobayashi | Zendy; Koji Shibuya | Zendy; Yoshihiro Tominaga | Zendy; Naoki Otsuki | Zendy; Kenichi Nibu | Zendy; Kimie Nakagawa | Zendy; Naoko Tsugawa | Zendy; Toshio Okano | Zendy; Riko Kitazawa | Zendy; Masafumi Fukagawa | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Depressed expression of Klotho and FGF receptor 1 in hyperplastic parathyroid glands from uremic patients

Author(s) -

Hirotaka Komaba,

Shunsuke Goto,

Hideki Fujii,

Yasuhiro Hamada,

Akira Kobayashi,

Koji Shibuya,

Yoshihiro Tominaga,

Naoki Otsuki,

Kenichi Nibu,

Kimie Nakagawa,

Naoko Tsugawa,

Toshio Okano,

Riko Kitazawa,

Masafumi Fukagawa

Publication year - 2009

Publication title -

kidney international

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.499

H-Index - 276

eISSN - 1523-1755

pISSN - 0085-2538

DOI - 10.1038/ki.2009.414

Subject(s) - klotho , endocrinology , medicine , fibroblast growth factor 23 , parathyroid hormone , immunohistochemistry , hyperparathyroidism , fibroblast growth factor receptor 1 , secondary hyperparathyroidism , hyperplasia , parathyroid gland , fibroblast growth factor , receptor , kidney , calcium

Fibroblast growth factor 23 (FGF23) exerts its effect by binding to its cognate FGF receptor 1 (FGFR1) in the presence of its co-receptor Klotho. Parathyroid glands express both FGFR1 and Klotho, and FGF23 decreases parathyroid hormone gene expression and hormone secretion directly. In uremic patients with secondary hyperparathyroidism (SHPT), however, parathyroid hormone secretion remains elevated despite extremely high FGF23 levels. To determine the mechanism of this resistance, we measured the expression of Klotho, FGFR1, and the proliferative marker Ki67 in 7 normal and 80 hyperplastic parathyroid glands from uremic patients by immunohistochemistry. All uremic patients had severe SHPT along with markedly high FGF23 levels. Quantitative real-time reverse transcription PCR showed that the mRNA levels for Klotho and FGFR1correlated significantly with their semi-quantitative immunohistochemical intensity. Compared with normal tissue, the immunohistochemical expression of Klotho and FGFR1 decreased, but Ki67 expression increased significantly in hyperplastic parathyroid glands, particularly in glands with nodular hyperplasia. These results suggest that the depressed expression of the Klotho-FGFR1 complex in hyperplastic glands underlies the pathogenesis of SHPT and its resistance to extremely high FGF23 levels in uremic patients.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research