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Knockdown of HCK promotes HREC cell viability and inner blood-retinal barrier integrity by regulating the AMPK

Lu Chen1, Chengmin Lin2

  • 1Ophthalmology Teaching and Research Office, Zhejiang Industry & Trade Vocational College, Wenzhou, Zhejiang, 325000, China.

Open Life Sciences
|September 9, 2024
PubMed

Insights

Hematopoietic cell kinase (HCK) shows increased expression in diabetic retinopathy (DR) under high glucose conditions. Targeting HCK may improve retinal cell viability and blood-retinal barrier integrity, offering new therapeutic strategies for DR.

Area of Science:

  • Ophthalmology
  • Endocrinology
  • Molecular Biology

Background:

  • Diabetic retinopathy (DR) is a leading cause of blindness due to diabetes-related retinal damage.
  • Current treatments for DR are limited, necessitating the identification of novel therapeutic targets.
  • Hematopoietic cell kinase (HCK) has emerged as a potential biomarker in DR, but its specific role is unclear.

Purpose of the Study:

  • To investigate the role of HCK in the progression of diabetic retinopathy.
  • To elucidate the underlying mechanisms of HCK action in high glucose-induced retinal damage.

Main Methods:

  • Human retinal capillary endothelial cells (HRECs) were cultured and exposed to high glucose (HG) conditions.
  • HCK expression levels were measured.
  • HCK was knocked down using specific techniques.
  • Cell viability and blood-retinal barrier integrity were assessed.
  • The AMPK pathway was analyzed in response to HCK depletion.

Main Results:

  • High glucose stimulation led to increased HCK expression in HRECs.
  • Knockdown of HCK significantly improved HREC cell viability.
  • HCK depletion enhanced the integrity of the internal blood-retinal barrier.
  • Suppression of the AMPK pathway was observed upon HCK depletion in HG-induced HRECs.

Conclusions:

  • HCK plays a significant role in the pathogenesis of diabetic retinopathy.
  • Targeting HCK presents a promising therapeutic strategy for DR.
  • HCK modulation impacts the AMPK pathway, offering a potential mechanism for treatment.

Keywords:
AMPK pathwayDRHCKHGinternal blood–retinal barrier

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