Experimental model for establishment of hypoxia in 75 cm² culture flasks

Keira, Sidney Mamoru; Ferreira, Lydia Masako; Gragnani, Alfredo; Duarte, Ivone da Silva; Campaner, Anelisa Bittencourt; Durão, Marcelino de Souza

doi:10.1590/s0102-86502004000700006

Cited by 2 publications

(2 citation statements)

References 5 publications

(1 reference statement)

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“…Hypoxia was established by maintaining culture flasks at 37°C under a constant flow of an hypoxic gas mixture composed of 95% N 2 and 5% CO 2 for 90 min as described. [27] Then flasks were sealed and incubated at 37°C for the desired time of hypoxia.…”

Section: Methodsmentioning

confidence: 99%

The Decrease of Mineralcorticoid Receptor Drives Angiogenic Pathways in Colorectal Cancer

et al. 2013

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Angiogenesis plays a crucial role in tumor growth and progression. Low expression of mineralocorticoid receptor (MR) in several malignant tumors correlates with disease recurrence and overall survival. Previous studies have shown that MR expression is decreased in colorectal cancer (CRC). Here we hypothesize that decreased MR expression can contribute to angiogenesis and poor patient survival in colorectal malignancies. In a cohort of CRC patients, we analyzed tumor MR expression, its correlation with tumor microvascular density and its impact on survival. Subsequently, we interrogated the role of MR in angiogenesis in an in vitro model, based on the colon cancer cell line HCT116, ingenierized to re-express a physiologically controlled MR. In CRC, decreased MR expression was associated with increased microvascular density and poor patient survival. In pchMR transfected HCT116, aldosterone or natural serum steroids largely inhibited mRNA expression levels of both VEGFA and its receptor 2/KDR. In CRC, MR activation may significantly decrease angiogenesis by directly inhibiting dysregulated VEGFA and hypoxia-induced VEGFA mRNA expression. In addition, MR activation attenuates the expression of the VEGF receptor 2/KDR, possibly dampening the activation of a VEGFA/KDR dependent signaling pathway important for the survival of tumor cells under hypoxic conditions.

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Section: Methodsmentioning

confidence: 99%

The Decrease of Mineralcorticoid Receptor Drives Angiogenic Pathways in Colorectal Cancer

et al. 2013

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“…Hypoxic preconditioning induces elevated expression of stanniocalcin-1 in the heart Submitted June 15, 2007; doi: 10.1152/ajpheart.00017.2007.-Animals exposed for a few hours to low oxygen content (8%) develop resistance against further ischemic myocardial damage. The molecular mechanism(s) behind this phenomenon, known as hypoxic preconditioning (HOPC), is still incompletely understood.…”

mentioning

confidence: 99%

Hypoxic preconditioning induces elevated expression of stanniocalcin-1 in the heart

Westberg¹,

Serlachius²,

Lankila³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Animals exposed for a few hours to low oxygen content (8%) develop resistance against further ischemic myocardial damage. The molecular mechanism(s) behind this phenomenon, known as hypoxic preconditioning (HOPC), is still incompletely understood. Stanniocalcin-1 (STC-1) is an evolutionarily conserved glycoprotein originally discovered in fish, in which it regulates calcium/phosphate homeostasis and protects against toxic hypercalcemia. Our group originally reported expression of mammalian STC-1 in brain neurons and showed that STC-1 is a prosurvival factor that guards neurons against hypercalcemic and hypoxic damage. This study investigates the involvement of STC-1 in HOPC-induced cardioprotection. Wild-type mice and IL-6-deficient (Il-6(-/-)) mice were kept in hypoxic conditions (8% O(2)) for 6 h. Myocardial Stc-1 mRNA expression was quantified during hypoxia and after recovery. HOPC triggered a biphasic upregulation of Stc-1 expression in hearts of wild-type mice but not in those of Il-6(-/-) mice. Treatment of cardiomyocyte cells in culture with hypoxia or IL-6 elicited an Stc-1 response, and ectopically expressed STC-1 in HL-1 cells localized to the mitochondria. Our findings indicate that IL-6-induced expression of STC-1 is one molecular mechanism behind the ischemic tolerance generated by HOPC in the heart.

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Experimental model for establishment of hypoxia in 75 cm² culture flasks

Cited by 2 publications

References 5 publications

The Decrease of Mineralcorticoid Receptor Drives Angiogenic Pathways in Colorectal Cancer

The Decrease of Mineralcorticoid Receptor Drives Angiogenic Pathways in Colorectal Cancer

Hypoxic preconditioning induces elevated expression of stanniocalcin-1 in the heart

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