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Review

Vaginal progesterone in risk reduction of preterm birth in women with short cervix in the midtrimester of pregnancy

Pages 481-490 | Published online: 14 Sep 2012

Figures & data

Table 1 Levels of prevention

Table 2 Clinically identifiable risk factors for spontaneous preterm birth

Table 3 Frequency of women with short cervix

Figure 1 Cholesterol is converted to pregnenolone by cytochrome P450scc inside steroidogenic mitochondria. The transport of cholesterol across the mitochondrial membranes is a limiting step, and it involves the transport protein (TSPO). Ligands of TSPO can stimulate the passage of cholesterol into the mitochondria and, as a consequence, the synthesis of pregnenolone. The conversion of pregnenolone to progesterone by different isoforms of the 3β-hydroxysteroid dehydrogenase (3β-HSD) also takes place inside the mitochondria or within the cytoplasm.

Notes: Progesterone regulates gene transcription by binding to intracellular receptors (PR), which interact as dimers with DNA progesterone-response elements (PREs). In addition, PR can also directly interact with extranuclear signaling proteins of the Src/Ras/Erk pathway. At the level of the plasma membrane, progesterone binds to the recently identified membrane receptors of progesterone (mPR, comprising a, b, and g isoforms), progesterone receptor membrane component 1 (PGRMC1, the former protein 25Dx) and the s1 receptor. Major signal transduction pathways which have been shown to be activated by the mPRs are ERK and p38. The mPRs also inhibit adenylate cyclase (AC), and as a consequence the protein kinase A (PKA) pathway, and they stimulate Ca2+ release from internal stores. Likewise, PGRMC1 and s1 receptors increase intracellular Ca2+ release. Both receptors are also located on membranes inside the cytoplasm, but they may translocate from them to the plasma membrane. In addition, PGRMC1 has been shown to activate protein kinase G (PKG), and s1 receptors function as amplifiers of ion channels (eg, voltage-gated K+ channels). Progesterone also activates γ-aminobutyric acid type A (GABAA) receptors via its metabolite allopregnanolone. Copyright © 2008, Elsevier. Reproduced with permission from Schumacher M, Sitruk-Ware R, De Nicola AF. Progesterone and progestins: neuroprotection and myelin repair. Curr Opin Pharmacol. 2008;8:740–746.Citation32
Abbreviation: 5αDHP, 5α dihydroprogesterone.
Figure 1 Cholesterol is converted to pregnenolone by cytochrome P450scc inside steroidogenic mitochondria. The transport of cholesterol across the mitochondrial membranes is a limiting step, and it involves the transport protein (TSPO). Ligands of TSPO can stimulate the passage of cholesterol into the mitochondria and, as a consequence, the synthesis of pregnenolone. The conversion of pregnenolone to progesterone by different isoforms of the 3β-hydroxysteroid dehydrogenase (3β-HSD) also takes place inside the mitochondria or within the cytoplasm.