TonEBP is a Master Regulator in Protection from Hyperosmolality in the Renal Medulla: Hypertonicity and Urea
نویسندگان
چکیده
ume by osmos C. elegans tol are first allow organic osmol tonicity (28). tonicity allow hypertonicity ic osmolytes o The process expression is i scription facto enhancer bind al regulator fo osmolytes (45 conditions, its ty rises (see be lar accumulati renal medulla membrane cotransperter cotransporter cotransporter enzymes—ald ropathy target glycerophosph 58). The organ sorbitol, and g inside the cel sized because In C. elega encodes glyce key event in th mulation (29) induction of g involved in the form of TonEB there is no To Despite the la sible that the m naling pathwa the stimulatio Urea also ca exceeds 300 m a role in prote by stimulating (HSP70) (49). HSP70 gene in and stimulate gle cell in the TonEBP (4, 30 by gene delet nant negative renal medulla hypertonicity threatening de water via urin ing ability. To medulla, where complex arrangements of tubules, some of which have regulated urea permeability, in combination with dynamics of counter current flow of tubular fluids confer osmotic effectiveness to urea for water reabsorption. In this discussion, however, we will ignore this and define hypertonicity as hyperosmotic salt because we will focus on cellular effects.
منابع مشابه
Hypertonicity and TonEBP promote development of the renal concentrating system.
DESPITE SEVERE HYPEROSMOTIC stress imposed by NaCl and urea on cells of the renal medulla, the elevated and highly variable osmolality in this part of the kidney is necessary for proper function of the urinary concentrating mechanism. This mechanism develops only after birth, and newborn rats are incapable of producing concentrated urine (13). Depending on hydration state, renal medullary osmol...
متن کاملUrea inhibits hypertonicity-inducible TonEBP expression and action.
Tonicity-responsive genes are regulated by the TonE enhancer element and the tonicity-responsive enhancer binding protein (TonEBP) transcription factor with which it interacts. Urea, a permeant solute coexistent with hypertonic NaCl in the mammalian renal medulla, activates a characteristic set of signaling events that may serve to counteract the effects of NaCl in some contexts. Urea inhibited...
متن کاملDNA damage signals facilitate osmotic stress adaptation.
OSMOTIC STRESS OCCURS WHEN the concentration of dissolved compounds in water surrounding cells and organisms changes. For example, changes in dissolved salt (inorganic ion) concentration in the environment are common for soil bacteria exposed to drought or rain, intertidal and estuary organisms facing fluctuating salinity, and kidney cells of the mammalian renal medulla. Osmotic changes in the ...
متن کاملSequential expression of NKCC2, TonEBP, aldose reductase, and urea transporter-A in developing mouse kidney.
This study was conducted to test the hypothesis that, during renal development, the Na-K-2Cl cotransporter type 2 (NKCC2) activates the tonicity-responsive enhancer binding protein (TonEBP) transcription factor by creating medullary hypertonicity. TonEBP, in turn, drives the expression of aldose reductase (AR) and urea transporter-A (UT-A). Kidneys from 13- to19-day-old fetuses (F13-F19), 1- to...
متن کاملModulation of TonEBP activity by SUMO modification in response to hypertonicity
TonEBP is a DNA binding transcriptional enhancer that enables cellular adaptation to hypertonic stress by promoting expression of specific genes. TonEBP expression is very high in the renal medulla because local hypertonicity stimulates its expression. Given the high level of expression, it is not well understood how TonEBP activity is modulated. Here we report that TonEBP is post-translational...
متن کامل