Figure 1.
PLS-DA score plot (3D) of PBMC cytokine gene expression between controls and primary dysmenorrhea groups.
DS, the secretory phase in the primary dysmenorrhea group (seventh day before menstruation); DM, the menstrual phase in the primary dysmenorrhea group (first day of menstruation); DP, the proliferative phase in the primary dysmenorrhea group (fifth day of menstruation); NS, NM, NP, the secretory, menstrual and proliferative phase, respectively, in unaffected controls.
Figure 2.
Multivariate analysis of cytokine gene expression profiles from controls (NM1-NM3) and dysmenorrheic (DM1–DM6) samples on the first day of menstruation.
A) Heat map showing hierarchical clustering of individual arrays by gene expression. B) 3D PCA score plot showing separate clustering of expression profiles corresponding to DM vs. NM. C) OPLS-DA model results for DM vs NM group. D) S-plot of OPLS-DA model for DM vs. NM group.
Table 1.
Genes revealed by quantitative RT-PCR analysis to be differentially expressed in women with primary dysmenorrhea on the seventh day before menstruation.
Table 2.
DAVID analysis of genes differentially expressed in women with primary dysmenorrhea on the seventh day before menstruation.
Table 3.
Functions and possible roles of genes differentially expressed in women with primary dysmenorrhea during the menstrual cycle.
Table 4.
Quantitative RT-PCR array analysis of differentially expressed genes in women with primary dysmenorrhea on the first day of menstruation.
Table 5.
DAVID analysis of differentially expressed genes in women with primary dysmenorrhea on the first day of menstruation.
Figure 3.
Expression of primary dysmenorrhea-related genes by quantitative RT-PCR array on the seventh day before menstruation, and the first and fifth days of menstruation.
Compared with the unaffected control group, the primary dysmenorrhea group has the relatively low expression of genes (BMP6, GDF5, GDF11, NODAL, IL1F5, IL11 and MSTN), and high expression of pro-inflammatory cytokines (IL1B, TNF, IL6, and IL8).
Figure 4.
A simplified representation of biological cross-talk between multiple TNFα/IL-1-induced actions and the TGF-β superfamily member signaling pathway.
TGF-β family members may interfere with the multiple roles of TNF-α/IL-1via HO-1, p300, PPARα, and PPARγ.
Figure 5.
A model of the biological basis of the onset of menstrual pain.
Menstruation is a response to the withdrawal of progesterone and depends on complex interactions between ovarian hormones and the immune system. A variety of immune factors not only regulate the inflammation and pain in menstruation, but also affect decidualization, tissue breakdown and early repair in the menstruation process. ↑, up-regulation of gene expression regulation; ↓, down-regulation of gene expression; (+), positive regulation; (−), negative regulation.
Table 6.
Quantitative RT-PCR array analysis of differentially expressed genes in women with primary dysmenorrhea on the fifth day of menstruation.
Table 7.
DAVID analysis of differentially expressed genes in women with primary dysmenorrhea on the fifth day of menstruation.