Skip to main content

Table 1 Genotyping and clinical information of AMD and control RPE, and patient’s skin fibroblasts from which the iPSC-RPE were generated

From: Repressed SIRT1/PGC-1α pathway and mitochondrial disintegration in iPSC-derived RPE disease model of age-related macular degeneration

Donor ID #

Donor age-gender (M: male; F: female)

Clinical diagnosis

CFH (C:risk)

HTRA1 (A:risk)

LOC (T:risk)

Factor B (T:protective)

C2 (C:protective)

Smoking

Cause of death

Time of enucleation (h)

Method of reprogramming

Tissue of origin

Generated iPSC-RPE

ID

R: RPE-iPSC-RPE

F:fibroblasts-iPSC-RPE

006

72-M

Control

CT

AG

GT

CC

GG

Quit in 1993

Chronic obstructive pulmonary disease

12

Sendai virus

RPE

6R

010

80-M

Control

CC

AG

GT

CC

GG

Quit in 1984

Acute myocardial infarction

9.4

Sendai virus

RPE

10R

025

50-M

Control

TT

GG

GG

CC

GG

No

Myocardial infarction

17

Sendai virus

RPE

25R

009

68-F

AMD

TT

GG

GG

TT

GG

2 ppd for 40 years

Stroke

3

Sendai virus

RPE

9R

032

75-M

AMD

CT

AA

TT

CC

GG

No

Pancreatic cancer

7

Sendai virus

RPE

32R

Patient ID

Patient age-gender (M: male; F: female)

Clinical diagnosis

CFH (C:risk)

FTRA1 (A:risk)

LOC (T:risk)

Factor B:(A:risk)

C2 (A:risk)

Smoking

     

Patient genotype

 005BF

80-F

AMD

CC

AG

GT

AA

CC

Quit in 1982 10 cigarettes pd for 20 years

Sendai virus

Fibroblasts

005BF

  1. The cause of death and time of enucleation are indicated. Cells were genotyped for known AMD-associated single nuclear polymorphisms (SNP) showing the haplotypes of each donor, carrying risk or protective alleles