Proteomic and bioinformatic analysis of human endometrium from polycystic ovarian syndrome with and without insulin resistance

Figures & data

Table 1. Baseline clinical and biochemical parameters in PCOS-IR, PCOS-non-IR, and control groups.

	Control (n = 7)	PCOS-non-IR (n = 12)	PCOS-IR (n = 21)	p value
Age (year)	27.00 ± 2.94	26.83 ± 2.533	25.24 ± 3.45	.246
BMI (kg/m^2)	21.39 ± 2.81	20.80 ± 2.42	26.10 ± 3.00	<.001
FSH (mIU/mL)	5.67 ± 0.83	6.78 ± 0.96	6.42 ± 1.82	.295
LH (mIU/mL)	5.34 ± 0.63	10.93 ± 5.37	10.45 ± 5.33	.045
T (ng/dL)	24.69 ± 11.36	38.8 ± 10.60	46.93 ± 17.65	.006
FBG (mmol/L)	4.54 ± 0.41	4.94 ± 0.55	5.10 ± 0.59	.001
FINS (mIU/mL)	8.97 ± 3.90	8.76 ± 11.77	24.68 ± 11.77	<.001
HOMA-IR	1.80 ± 0.80	1.94 ± 0.52	5.90 ± 2.94	<.001
CHO (mmol/L)	3.65 ± 0.81	3.86 ± 0.75	4.17 ± 0.74	.279
TG (mmol/L)	0.99 ± 0.43	1.03 ± 0.63	1.85 ± 0.95	.013
HDL-C (mmol/L)	1.45 ± 0.43	1.47 ± 0.24	1.14 ± 0.25	.007
LDL-C (mmol/L)	2.22 ± 0.52	2.44 ± 0.56	2.82 ± 0.71	.110
TSH (μIU/mL)	3.44 ± 2.22	2.61 ± 1.03	3.12 ± 1.51	.501
IP (mouth)	5.29 ± 1.60	8.42 ± 4.38	9.05 ± 2.69	.033
Live birth rate	7/7 (100.00%)	10/12 (83.33%)	10/21 (47.62%)	.014

BMI: body mass index; FSH: follicle-stimulating hormone; LH: luteinizing hormone; T: testosterone; FBG: fasting blood glucose; FINS: fasting insulin; HOMA-IR: homeostasis model assessment of insulin resistance; CHO: cholesterol; TG: triglyceride; HDL-C: high-density lipoprotein cholesterol; LDL-C: low-density lipoprotein cholesterol; TSH: thyroid stimulating hormone; IP: interval between the time of endometrial collection and the time of final pregnancy.

p < .05 was considered statistically significant.

Figure 1. Sample expression correction box diagram and volcano diagram. A: Protein expression before normalization. B: Protein expression after sample normalization. The red sample represents the PCOS-non-IR group, the green sample represents the PCOS-IR group and the blue sample represents the control group. C: PCOS vs. Control. D: PCOS-IR vs. PCOS-non-IR. (Red dots represent up-regulated differential proteins, green dots represent down-regulated proteins, and no significantly changed genes are marked as gray dots).

Figure 2. PCOS vs. Control: GO and KEGG enrichment of differentially expressed proteins (DEPs). (A) biological process, (B) cellular component, (C) molecular function, and (D) KEGG pathway analysis.

Figure 3. PCOS-IR vs. PCOS-non-IR: GO and KEGG enrichment of differentially expressed proteins (DEPs). (A) biological process, (B) cellular component, (C) molecular function, and (D) KEGG pathway analysis.

Figure 4. A: Venn diagrams to visually display the intersection of differential proteins between PCOS vs. control and PCOs-IR vs. PCOs-non-IR groups. B: PCA between the PCOS-IR, PCOS-non-IR and control groups. The red sample represents the PCOS-non-IR group, the green sample represents the PCOS-IR group and the blue sample represents the control group. C and D: The LASSO regression model for live birth of PCOS-IR patients. E: ROC of different factors on pregnancy outcome.

Figure 5. Analysis of key proteins expression: (A, B, E) ACTR1A and CKB were higher in PCOS-IR group, while TSC22D2 was lower in PCOS-IR group (p < .05). (C and D) ABRAXAS2 was higher in all PCOS groups and TAGLN2 was low in all PCOS groups (p < .05), but there was no difference between the PCOS-IR and PCOS-non-IR groups (p > .05). Pearson correlation analysis between key proteins and HOMA-IR: (F and G) ACTR1A and CKB was significantly positively correlated with HOMA-IR. (H, I, and J) there was no significant correlation between TAGLN2, ABRAXAS2 and TSC22D2 with HOMA-IR.

Availability of data and materials

The Trial data used in this manuscript have been deposited to the Proteome Xchange Consortium (http://proteomecentral.proteomexchange.org) via the iProX partner repository with the dataset identifier PXD032383.