Of these options available, Schwann cells would be the only cells present in the PNS. Astrocytes, microglia and oligos are all CNS cells Satellite cells are in the muscle and serve to aid in muscle repair and regeneration

Schwann cells: they are supposed to degrade residual myelin sheath during the neuronal degeneration. Without that degeneration, I guess you can’t re-innervate properly. Not totally sure.

There’s a UWorld question on this. Once the healthy axon retracts and the distal (injured) axon degenerates, there’s a bunch of myelin debris in the way that remains there for a long time. This blocks regeneration of the axon.

Central nervous system regeneration

Unlike peripheral nervous system injury, injury to the central nervous system is not followed by extensive regeneration. It is limited by the inhibitory influences of the glial and extracellular environment. The hostile, non-permissive growth environment is, in part, created by the migration of myelin-associated inhibitors, astrocytes, oligodendrocytes, oligodendrocyte precursors, and microglia. The environment within the CNS, especially following trauma, counteracts the repair of myelin and neurons. Growth factors are not expressed or re-expressed; for instance, the extracellular matrix is lacking laminins. Glial scars rapidly form, and the glia actually produce factors that inhibit remyelination and axon repair; for instance, NOGO and NI-35.The axons themselves also lose the potential for growth with age, due to a decrease in GAP43 expression, among others.

Wallerian Degeneration : axonal degeneration distal to site of transection + proximal axonal retraction

Axotomy (axonal tran-section) of peripheral nerves results in, Schwann cells : a. breaking down myelin into small fragments and englufs it b. recruiting macrophages to dispose of axonal debri c. producing growth factors to promote regeneration of axons

Neuroregeneration in the peripheral nervous system (PNS) occurs to a significant degree.[5][6] After an injury to the axon, peripheral neurons activate a variety of signaling pathways which turn on pro-growth genes, leading to reformation of a functional growth cone and regeneration. The growth of these axons is also governed by chemotactic factors secreted from Schwann cells. Injury to the peripheral nervous system immediately elicits the migration of phagocytes, Schwann cells, and macrophages to the lesion site in order to clear away debris such as damaged tissue which is inhibitory to regeneration. When a nerve axon is severed, the end still attached to the cell body is labeled the proximal segment, while the other end is called the distal segment. After injury, the proximal end swells and experiences some retrograde degeneration, but once the debris is cleared, it begins to sprout axons and the presence of growth cones can be detected. The proximal axons are able to regrow as long as the cell body is intact, and they have made contact with the Schwann cells in the endoneurial channel or tube. Human axon growth rates can reach 2 mm/day in small nerves and 5 mm/day in large nerves.[4] The distal segment, however, experiences Wallerian degeneration within hours of the injury; the axons and myelin degenerate, but the endoneurium remains. In the later stages of regeneration the remaining endoneurial tube directs axon growth back to the correct targets. During Wallerian degeneration, Schwann cells grow in ordered columns along the endoneurial tube, creating a band of Büngner (boB) that protects and preserves the endoneurial channel. Also, macrophages and Schwann cells release neurotrophic factors that enhance re-growth.

(wiki)