Sanele Khoza

Dr. Sanele Khoza

Primate Unit and Delft Animal Centre, South African Medical Research Council, Cape Town, Western Cape, South Africa
orcid

Research Focus & Metrics

Academic Career Length

8Years (2019-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
23 January 2020 in Journal of Medical Primatology
Verified
Journal Article
Closed access
PDF file
TNThobile Ngqaneka
Thobile Ngqaneka
SKSanele Khoza
Sanele Khoza
ZMZandisiwe Emilia Magwebu
Zandisiwe Emilia Magwebu
CCChesa G. Chauke
Chesa G. Chauke
1

6 February 2019 in Journal of Medical Primatology
Verified
Journal Article
Closed access
PDF file
SKSanele Khoza
Sanele Khoza
TNThobile Ngqaneka
Thobile Ngqaneka
ZMZandisiwe Emilia Magwebu
Zandisiwe Emilia Magwebu
CCChesa Gift Chauke
Chesa Gift Chauke
1

17 February 2023 in Advances in Cell and Gene Therapy
Verified
Journal Article
Open access
PDF file
SKSanele Khoza
Sanele Khoza
MGMeenu Ghai
Meenu Ghai
CCChesa G. Chauke
Chesa G. Chauke
ZMZandisiwe Emilia Magwebu
Zandisiwe Emilia Magwebu
Mendelian genetics contribute largely to the development of hypertension; therefore, the identification of genetic variants related to blood pressure (BP) regulation remains crucial and may reveal new therapeutic drug targets. The purpose of the present study was to screen the captive-bred Vervet colony for salt-sensitive sequence variants or single nucleotide polymorphisms (SNPs) in the selected Renin-Angiotensin-Aldosterone System (RAAS) genes associated with salt sensitivity. Blood samples were collected from 16 captive-bred Vervet monkeys for genotyping and gene expression analysis. The impact of the identified sequence variants was determined using online prediction tools. Sanger sequencing analysis revealed 21 sequence variants in AGT, CYP3A5, GRK4, and SCL4A5, of which 19 were novel and two were previously reported in humans. All novel variants were either predicted to be polymorphic, disease-causing, or possibly damaging by prediction tools. Furthermore, the mRNA expression for AGT was significantly higher in the normal BP group ( value = 0.02), and a similar trend was observed for CYP3A5 and GRK4, whereas SCL4A5 was higher in the hypertensive group. The identified salt-sensitive variants specifically in GRK4 may be suggestive to be the attributing factor of the elevated BP levels in these captive-bred Vervet monkeys. Therefore, RAAS variants could be considered as a biomarker to identify the potential risk of developing hypertension in both humans and nonhuman primates.
1