Table 1 Summary of Gene Set Enrichment Analysis (GSEA) used to identify pathways affected by loss of Brn-3b in the aorta.

From: Vascular dysfunction caused by loss of Brn-3b/POU4F2 transcription factor in aortic vascular smooth muscle cells is linked to deregulation of calcium signalling pathways

a

GSEA analysis: Upregulated genes (KEGG Pathways)

NES

Genes

adj.Pval

Calcium Signalling and Muscle contraction

Calcium signalling pathway

1.5097

158

3.30E-04

CAMP signalling pathway

1.4551

146

3.30E-04

Adrenergic signalling in cardiomyocytes

1.5349

119

3.30E-04

Oxytocin signalling pathway

1.4507

114

8.00E-04

Vascular smooth muscle contraction

1.4459

93

4.20E-03

Neuroactive ligand-receptor interaction

1.4483

90

4.20E-03

Dilated cardiomyopathy

1.6415

79

3.30E-04

Hypertrophic cardiomyopathy

1.6252

74

3.30E-04

Aldosterone synthesis and secretion

1.4714

72

5.10E-03

Cardiac muscle contraction

1.7434

65

3.30E-04

Arrhythmogenic right ventricular cardiomyopathy

1.6189

64

3.30E-04

Circadian pathways

Circadian entrainment

1.6437

68

3.30E-04

Circadian rhythm

1.8517

25

3.30E-04

Immune response and Haematopoiesis

Hematopoietic cell lineage

1.4943

57

6.20E-03

IL-17 signalling pathway

1.4874

56

7.70E-03

Viral protein interaction - cytokine & cytokine receptor

1.5198

43

9.40E-03

Malaria

1.4702

29

6.20E-02

Metabolic Processes

Pancreatic secretion

1.4943

61

5.50E-03

Cortisol synthesis and secretion

1.4363

47

3.60E-02

Regulation of lipolysis in adipocytes

1.4939

46

1.40E-02

GnRH secretion

1.528

44

8.50E-03

Long-term depression

1.4447

44

3.70E-02

Metabolism of xenobiotics by cytochrome P450

1.6406

39

1.80E-03

Chemical carcinogenesis

1.656

38

1.50E-03

Drug metabolism

1.5963

36

5.10E-03

Type II diabetes mellitus

1.4488

34

6.20E-02

Tryptophan metabolism

1.6074

25

1.40E-02

Retinol metabolism

1.6941

22

5.10E-03

One carbon pool by folate

1.4936

15

1.30E-01

b

GSEA analysis Down regulated (KEGG Pathway)

NES

Genes

adj.Pval

VSMC and muscle contraction

Regulation of actin cytoskeleton

−1.7531

40

2.0e-01

Vascular smooth muscle contraction

−1.6927

35

2.3e-01

Apelin signalling pathway

−1.7974

33

2.0e-01

Immune response and Haematopoiesis

Chemokine signalling pathway

−1.9784

37

8.4e-02

Cytokine-cytokine receptor interaction

−1.7391

37

2.0e-01

IL-17 signalling pathway

−2.0966

16

8.4e-02

Alzheimer disease

−2.0803

15

8.4e-02

Hematopoietic cell lineage

−1.8507

15

2.0e-01

Human cytomegalovirus infection

−1.6782

41

2.3e-01

Other processes

Oxytocin signalling pathway

−1.6876

34

2.3e-01

Prostate cancer

−1.9581

17

1.7e-01

Bladder cancer

−1.8539

10

2.0e-01

(c): JENSEN Disease pathways: Upregulated genes

GSEA analysis: KO vs WT

NES

Genes

adj.Pval

Hypertension

1.4752

169

4.20E-04

Coronary artery disease

1.5283

128

4.20E-04

Arthritis

1.5689

115

4.20E-04

Cardiomyopathy

1.67

75

4.20E-04

Obesity

1.4581

68

1.50E-02

Congenital heart disease

1.4512

50

5.10E-02

Pneumonia

1.5689

37

1.50E-02

Major depressive disorder

1.4563

35

8.10E-02

Hyperinsulinism

1.4617

33

8.50E-02

Dilated cardiomyopathy

1.6009

31

1.50E-02

Distal arthrogryposis

1.7376

30

7.30E-04

Atrial fibrillation

1.5199

30

5.50E-02

Infertility

1.4683

29

9.40E-02

Eosinophilia

1.4631

27

1.00E-01

Pulmonary embolism

1.4986

23

9.40E-02

Meningitis

1.5829

22

5.20E-02

Hemochromatosis

1.5156

21

9.40E-02

Lymphedema

1.5966

20

5.20E-02

DOID:9917

1.5509

20

8.00E-02

Polyneuropathy

1.513

20

9.40E-02

Hyperhomocysteinemia

1.4927

20

1.10E-01

Leukopenia

1.4853

19

1.20E-01

Malignant hyperthermia

1.9492

18

4.20E-04

Pre-eclampsia

1.5755

17

8.00E-02

Candidiasis

1.4921

17

1.20E-01

Hypertrophic cardiomyopathy

1.6314

16

5.10E-02

Essential tremor

1.4935

16

1.20E-01

Hyperthyroidism

1.654

15

4.60E-02

Primary cutaneous amyloidosis

1.5242

15

1.10E-01

Hypokalemia

1.5129

15

1.20E-01

  1. GSEA data showing functional KEGG pathways associated with genes that were either (a) upregulated or (b) down regulated in Brn-3b KO aortas, when compared with WT controls. Significance was determined using the normalisation enrichment scores (NES), number of genes and adjusted p value. NES [(+) = increased expression; (−) = down-regulated genes in Brn-3b KO tissue. (c) Summary of Jensen.disease pathway analysis to identify effects caused by genes that were significantly and when compared with WT controls differentially expressed genes in Brn-3b KO mutants.
  2. Bold text represent the subheadings to highlight distinct pathways affected in mutant aorta compared with WTcontrols.
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