1,25-Dihydroxyvitamin D3 maintains adherence of human monocytes and protects them from thermal injury

B S Polla , A M Healy , E P Amento

The Journal of Clinical Investigation +

|

April 1, 1986

View abstract on PubMed

Summary

1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) preserves monocyte adherence by maintaining protein synthesis, even under thermal stress. This vitamin D metabolite also enhances heat shock protein production, aiding monocyte survival and function.

Area Of Science

Immunology
Cell Biology
Endocrinology

Background

Monocyte-macrophage adherence to substrata is crucial for effector functions.
Monocytes exhibit transient adherence to fibronectin and biological matrices.
Loss of monocyte adherence occurs despite maintained cell viability.

Purpose Of The Study

To investigate the role of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) in maintaining monocyte adherence.
To explore the effects of 1,25-(OH)2D3 on monocyte protein synthesis and response to thermal stress.

Main Methods

Monocyte adherence assays to fibronectin and biological matrices.
Cell viability assessments using trypan blue exclusion and LDH release.
Protein synthesis analysis via [35S]methionine labeling and 2D gel electrophoresis.
Evaluation of 1,25-(OH)2D3 effects under thermal stress (45°C).

Main Results

1,25-(OH)2D3 maintained monocyte adherence in a concentration- and time-dependent manner.
1,25-(OH)2D3 treatment increased the synthesis of specific cellular proteins.
1,25-(OH)2D3 partially prevented adherence loss and protein synthesis reduction under thermal stress.
1,25-(OH)2D3 enhanced heat shock protein synthesis and recovery of protein synthesis post-stress.

Conclusions

1,25-(OH)2D3 preserves monocyte adherence by sustaining protein synthesis.
This vitamin D metabolite influences monocyte function through protein synthesis modulation.
1,25-(OH)2D3 confers protection against thermal stress by enhancing heat shock protein synthesis.

Related Concept Videos