TY - JOUR
T1 - 3, 5, 3'-Triiodothyronine determines the viability of gc cells after heat shock
AU - Shapiro, Lawrence E.
AU - Wasserman, Susan H.Scherf
AU - Katz, Claire P.
AU - Surks, Martin I.
PY - 1989/2
Y1 - 1989/2
N2 - The heat shock (HS) response is a characteristic disruption of protein synthesis which occurs in cells exposed to a variety of noxious stimuli. The effects of HS on thyroid hormone-responsive GC cells were studied in an attempt to devise an in vitro model for the adaptive changes in thyroid hormone action caused by nonthyroidal disease. HS enhanced GC cell synthesis of 70 K and 90 K proteins in a manner previously described as characteristic of the HS response in many tissues. A step-wise decrease in GC cell viability occurred when cells were exposed to 45 C for 10 to 35 min. HS (45 C, 20 min) resulted in a rapid decrease in binding of T3 to nuclear receptors. Two hours after HS, analysis of T3 binding to isolated nuclei showed a 50% fall in binding capacity (240 fmol/100 μg DNA) compared to non-HS control cells (540 fmol/100 μg DNA); no difference in dissociation constant (Kd) was observed. The effect of thyroid hormone on cell viability after HS was then determined. Thyroid hormone depletion (≪0.02 nM T3) resulted in significantly (P ≪ 0.05) enhanced cell viability compared to cells cultured with physiological T3 (0.2 nM) after incubation at 45 C for intervals of 10-35 min. This inverse relationship between medium T3 content and cell tolerance of HS occurred over a wide range of T3 concentrations. Mean cell viability after exposure to 45 C for 20 min was 44 ± 3% in T3-depleted cultures (≪0.02 nM), 27 ± 1% to 32 ± 5% in cultures containing 0.07-0.5 nM T3, and 13 ± 3% in cultures containing 5 nM T3. Our results thus characterize the response to HS in GC cells and the relationship of this response to medium T3. Similar to the effect of various nonthyroidal diseases on rat hepatocytes in vivo, HS resulted in a decrease in T3 nuclear receptors. Similar to the adverse effect of thyroid hormone on morbidity in animals with experimental diseases or injury, GC cell viability after HS was inversely related to medium T3 content. Thus the HS response in GC cells may be a valuable in vitro model relevant to the effect on thyroid hormone action caused by nonthyroidal disease.
AB - The heat shock (HS) response is a characteristic disruption of protein synthesis which occurs in cells exposed to a variety of noxious stimuli. The effects of HS on thyroid hormone-responsive GC cells were studied in an attempt to devise an in vitro model for the adaptive changes in thyroid hormone action caused by nonthyroidal disease. HS enhanced GC cell synthesis of 70 K and 90 K proteins in a manner previously described as characteristic of the HS response in many tissues. A step-wise decrease in GC cell viability occurred when cells were exposed to 45 C for 10 to 35 min. HS (45 C, 20 min) resulted in a rapid decrease in binding of T3 to nuclear receptors. Two hours after HS, analysis of T3 binding to isolated nuclei showed a 50% fall in binding capacity (240 fmol/100 μg DNA) compared to non-HS control cells (540 fmol/100 μg DNA); no difference in dissociation constant (Kd) was observed. The effect of thyroid hormone on cell viability after HS was then determined. Thyroid hormone depletion (≪0.02 nM T3) resulted in significantly (P ≪ 0.05) enhanced cell viability compared to cells cultured with physiological T3 (0.2 nM) after incubation at 45 C for intervals of 10-35 min. This inverse relationship between medium T3 content and cell tolerance of HS occurred over a wide range of T3 concentrations. Mean cell viability after exposure to 45 C for 20 min was 44 ± 3% in T3-depleted cultures (≪0.02 nM), 27 ± 1% to 32 ± 5% in cultures containing 0.07-0.5 nM T3, and 13 ± 3% in cultures containing 5 nM T3. Our results thus characterize the response to HS in GC cells and the relationship of this response to medium T3. Similar to the effect of various nonthyroidal diseases on rat hepatocytes in vivo, HS resulted in a decrease in T3 nuclear receptors. Similar to the adverse effect of thyroid hormone on morbidity in animals with experimental diseases or injury, GC cell viability after HS was inversely related to medium T3 content. Thus the HS response in GC cells may be a valuable in vitro model relevant to the effect on thyroid hormone action caused by nonthyroidal disease.
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U2 - 10.1210/endo-124-2-1026
DO - 10.1210/endo-124-2-1026
M3 - Article
C2 - 2912682
AN - SCOPUS:0024537116
SN - 0013-7227
VL - 124
SP - 1026
EP - 1032
JO - Endocrinology
JF - Endocrinology
IS - 2
ER -