Physiological Lactate Stress Reveals a β1.2- Dependent Protective Effect in Kv1.5 Expressing HEK293T Cells

Molitor, Frankie

Permalink

https://hdl.handle.net/2142/133171 Copy

Description

Title

Physiological Lactate Stress Reveals a β1.2- Dependent Protective Effect in Kv1.5 Expressing HEK293T Cells

Author(s)

Molitor, Frankie

Contributor(s)

Zinkevich, Natalya

Issue Date

2026

Keyword(s)

lactate, metabolic stress, cell density

Date of Ingest

2026-05-05T09:27:37-05:00

Abstract

Lactate was traditionally viewed as only a metabolic waste product, but emerging cardiovascular research shows cells can use it as both an energy source and a signaling molecule during stress. During ischemia, hypoxia, or accelerated glycolysis, lactate can rise to physiologic concentrations between 5-10 mM, influencing ion channel behavior, oxidative stress responses, and cell survival. Kv1.5, a voltage-gated potassium channel expressed in atrial cardiomyocytes and vascular smooth muscle cells, interacts with auxiliary beta-subunits such as β1.2. However, it remains unclear whether β1.2 changes cellular responses to metabolic stress signals like lactate. Addressing this, we conducted a study investigating whether β1.2 alters cell survival under physiological levels of lactate. Human embryonic kidney 293T (HEK293T) cells expressing neither Kv1.5 nor β1.2 (control cells), HEK293T cells expressing Kv1.5 only, and HEK293T cells expressing both Kv1.5 and β1.2 were grown under standard conditions (37°C, 5% CO₂). All three groups underwent exposure to 8 mM lactate for 30 minutes. For each trial (n=4), four “before” and four “after” images were taken for both no-treatment control and lactate conditions. ImageJ will be used to quantify cell density changes. Preliminary imaging results showed a consistent pattern across trials: control and Kv1.5-only expressing cells demonstrated decreased cell density upon lactate exposure, while Kv1.5+β1.2 cells expressing cells have maintained cell density post-treatment. No changes occurred in no-treatment conditions for any group. These findings suggest β1.2 may confer protection against lactate-induced metabolic stress. Future studies will further define β1.2’s role in conditions where lactate accumulates.

Type of Resource

text

Genre of Resource

conference presentation

Language

eng

Sponsor(s)/Grant Number(s)

Brookens Library

Copyright and License Information

Author, 2026

Owning Collections